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1
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Krupa H, Gearhardt AN, Lewandowski A, Avena NM. Food Addiction. Brain Sci 2024; 14:952. [PMID: 39451967 PMCID: PMC11506718 DOI: 10.3390/brainsci14100952] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/31/2024] [Revised: 09/12/2024] [Accepted: 09/19/2024] [Indexed: 10/26/2024] Open
Abstract
In this review, we aim to draw a connection between drug addiction and overconsumption of highly palatable food (OHPF) by discussing common behaviors and neurochemical pathways shared by these two states. OHPF can stimulate reward pathways in the brain that parallel those triggered by drug use, increasing the risk of dependency. Behavioral similarities between food and drug addiction can be addressed by tracking their stages: loss of control when eating (bingeing), withdrawal, craving, sensitization, and cross-sensitization. The brain adapts to addiction by way of the mesolimbic dopamine system, endogenous opioids and receptors, acetylcholine and dopamine balance, and adaptations of serotonin in neuroanatomy. Studies from the current literature are reviewed to determine how various neurological chemicals contribute to the reinforcement of drug addiction and OHPF. Finally, protocols for treating food addiction are discussed, including both clinical and pharmacological modalities. There is consistent evidence that OHPF changes brain chemistry and leads to addiction in similar ways to drugs. However, more long-term research is needed on food addiction, binge eating, and their neurobiological effects.
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Affiliation(s)
- Haley Krupa
- Marian Regional Medical Center, Santa Maria, CA 93454, USA;
| | | | | | - Nicole M. Avena
- Icahn School of Medicine at Mount Sinai, New York, NY 10021, USA
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2
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Hu S, Gearhardt AN, LaFata EM. Development of the modified Highly Processed Food Withdrawal Scale (mProWS). Appetite 2024; 198:107370. [PMID: 38653374 DOI: 10.1016/j.appet.2024.107370] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/01/2023] [Revised: 04/19/2024] [Accepted: 04/20/2024] [Indexed: 04/25/2024]
Abstract
The Highly Processed Food Withdrawal Scale (ProWS) is a 29-item measure that operationalizes physical and psychological indicators of withdrawal symptoms associated with cutting down on the consumption of ultra-processed foods. The current study developed a briefer 7-item version of the ProWS (modified ProWS; mProWS) using the participant sample from the ProWS validation paper (n = 231). Then, in an independent sample recruited from Amazon Mechanical Turk, 244 participants (55.3% females) completed the mProWS, the ProWS, and measures of eating-related constructs in order to evaluate the psychometric properties of the mProWS, relative to the ProWS. The mProWS and the ProWS performed similarly on indexes of reliability, convergent validity with addictive-like eating behavior (e.g., Yale Food Addiction Scale 2.0 symptom count), discriminant validity with distinct measures (e.g., cognitive desire to restrict food consumption), and incremental validity evidenced by associations with weight cycling above and beyond body mass index (BMI) and YFAS 2.0 symptoms. The mProWS may be an appropriate choice for studies with higher participant burden (e.g., ecological momentary assessment) to assess withdrawal symptoms in real-time when they occur in response to cutting down on ultra-processed foods.
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Affiliation(s)
- Shuchen Hu
- Department of Clinical and Counseling Psychology, Teachers College, Columbia University, New York, NY, USA.
| | | | - Erica M LaFata
- Center for Weight, Eating and Lifestyle Science (WELL Center), Drexel University, Philadelphia, PA, USA.
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3
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Gancarz AM, Parmar R, Shwani T, Cobb MM, Crawford MN, Watson JR, Evans L, Kausch MA, Werner CT, Dietz DM. Adolescent exposure to sucrose increases cocaine-mediated behaviours in adulthood via Smad3. Addict Biol 2023; 28:e13346. [PMID: 38017636 DOI: 10.1111/adb.13346] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/29/2023] [Revised: 09/21/2023] [Accepted: 09/22/2023] [Indexed: 11/30/2023]
Abstract
Adolescence, a critical period of developmental period, is marked by neurobiological changes influenced by environmental factors. Here, we show how exposure to sucrose, which is ubiquitously available in modern diets, results in changes in behavioural response to cocaine as an adult. Rats were given daily access to either 10% sucrose or water during the adolescent period (PND28-42). Following this period, rats are left undisturbed until they reach adulthood. In adulthood, rats were tested for (i) acquisition of a low dose of cocaine, (ii) progressive ratio (PR) test, and (iii) resistance to punished cocaine taking. Sucrose exposure resulted in significant alterations in all behavioural measures. To determine the neurobiological mechanisms leading to such behavioural adaptations, we find that adolescent sucrose exposure results in an upregulation of the transcription factor Smad3 in the nucleus accumbens (NAc) when compared with water-exposed controls. Transiently blocking the active form of this transcription factor (HSV-dnSmad3) during adolescence mitigated the enhanced cocaine vulnerability-like behaviours observed in adulthood. These findings suggest that prior exposure to sucrose during adolescence can heighten the reinforcing effects of cocaine. Furthermore, they identify the TGF-beta pathway and Smad3 as playing a key role in mediating enduring and long-lasting adaptations that contribute to sucrose-induced susceptibility to cocaine. Taken together, these results have important implications for development and suggest that adolescent sucrose exposure may persistently enhance the susceptibility to substance abuse.
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Affiliation(s)
- Amy M Gancarz
- Department of Psychology, California State University, Bakersfield, California, USA
- Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA
- Clinical and Research Institute on Addictions, University at Buffalo, Buffalo, New York, USA
| | - Raveena Parmar
- Department of Psychology, California State University, Bakersfield, California, USA
| | - Treefa Shwani
- Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA
| | - Moriah M Cobb
- Department of Psychology, California State University, Bakersfield, California, USA
| | - Michelle N Crawford
- Department of Psychology, California State University, Bakersfield, California, USA
| | - Jacob R Watson
- Department of Psychology, California State University, Bakersfield, California, USA
| | - Lisa Evans
- Department of Psychology, California State University, Bakersfield, California, USA
| | - Michael A Kausch
- Department of Psychology, California State University, Bakersfield, California, USA
- Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA
| | - Craig T Werner
- Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA
| | - David M Dietz
- Department of Pharmacology and Toxicology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, Buffalo, New York, USA
- Clinical and Research Institute on Addictions, University at Buffalo, Buffalo, New York, USA
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4
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Hamamah S, Hajnal A, Covasa M. Reduced Striatal Dopamine Transporter Availability and Heightened Response to Natural and Pharmacological Stimulation in CCK-1R-Deficient Obese Rats. Int J Mol Sci 2023; 24:ijms24119773. [PMID: 37298724 DOI: 10.3390/ijms24119773] [Citation(s) in RCA: 2] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/29/2023] [Revised: 05/28/2023] [Accepted: 06/03/2023] [Indexed: 06/12/2023] Open
Abstract
Alterations in dopamine neurotransmission are associated with obesity and food preferences. Otsuka Long-Evans Tokushima Fatty (OLETF) rats that lack functional cholecystokinin receptor type-1 (CCK-1R), due to a natural mutation, exhibit impaired satiation, are hyperphagic, and become obese. In addition, compared to lean control Long-Evans Tokushima (LETO) rats, OLETF rats have pronounced avidity for over-consuming palatable sweet solutions, have greater dopamine release to psychostimulants, reduced dopamine 2 receptor (D2R) binding, and exhibit increased sensitivity to sucrose reward. This supports altered dopamine function in this strain and its general preference for palatable solutions such as sucrose. In this study, we examined the relationship between OLETF's hyperphagic behavior and striatal dopamine signaling by investigating basal and amphetamine stimulated motor activity in prediabetic OLETF rats before and after access to sucrose solution (0.3 M) compared to non-mutant control LETO rats, as well as availability of dopamine transporter (DAT) using autoradiography. In the sucrose tests, one group of OLETF rats received ad libitum access to sucrose while the other group received an amount of sucrose equal to that consumed by the LETO. OLETFs with ad libitum access consumed significantly more sucrose than LETOs. Sucrose exerted a biphasic effect on basal activity in both strains, i.e., reduced activity for 1 week followed by increased activity in weeks 2 and 3. Basal locomotor activity was reduced (-17%) in OLETFs prior to sucrose, compared to LETOs. Withdrawal of sucrose resulted in increased locomotor activity in both strains. The magnitude of this effect was greater in OLETFs and the activity was increased in restricted compared to ad-libitum-access OLETFs. Sucrose access augmented AMPH-responses in both strains with a greater sensitization to AMPH during week 1, an effect that was a function of the amount of sucrose consumed. One week of sucrose withdrawal sensitized AMPH-induced ambulatory activity in both strains. In OLETF with restricted access to sucrose, withdrawal resulted in no further sensitization to AMPH. DAT availability in the nucleus accumbens shell was significantly reduced in OLETF compared with aged-matched LETO. Together, these findings show that OLETF rats have reduced basal DA transmission and a heightened response to natural and pharmacological stimulation.
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Affiliation(s)
- Sevag Hamamah
- Department of Basic Medical Sciences, College of Osteopathic Medicine, Western University of Health Sciences, Pomona, CA 91766, USA
| | - Andras Hajnal
- Department of Neural and Behavioral Sciences, College of Medicine, The Pennsylvania State University, Hershey, PA 17033, USA
| | - Mihai Covasa
- Department of Basic Medical Sciences, College of Osteopathic Medicine, Western University of Health Sciences, Pomona, CA 91766, USA
- Department of Biomedical Sciences, College of Medicine and Biological Science, University of Suceava, 720229 Suceava, Romania
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Abstract
Food addiction is associated with dysfunctions in the reward circuit, such as hyperresponsiveness during the exposure to high-calorie flavors in overweight and obese individuals. Similar to drug addiction, there is also impaired self-regulatory control supported by deregulation of the frontostriatal circuit. The inclusion of validated measures of food addiction in clinical research, such as the Yale Food Addiction Scale, has increased the understanding of the clinical utility of this concept. Furthermore, food addiction, eating disorders, and obesity are interrelated. Thus, it is important to recognize food addiction among individuals affected by obesity and candidates for bariatric surgery (ie, preoperative and postoperative assessment). In this context, it has been reported that food addiction may impede weight loss and increase the likelihood of regaining weight when associated with personality traits such as neuroticism and impulsiveness, which are also related to mood disorders, anxiety, and addictive behaviors.
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O'Connor RM, Kenny PJ. Utility of 'substance use disorder' as a heuristic for understanding overeating and obesity. Prog Neuropsychopharmacol Biol Psychiatry 2022; 118:110580. [PMID: 35636576 DOI: 10.1016/j.pnpbp.2022.110580] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/31/2022] [Revised: 05/24/2022] [Accepted: 05/24/2022] [Indexed: 02/07/2023]
Abstract
Rates of obesity and obesity-associated diseases have increased dramatically in countries with developed economies. Substance use disorders (SUDs) are characterized by the persistent use of the substance despite negative consequences. It has been hypothesized that overconsumption of palatable energy dense food can elicit SUD-like maladaptive behaviors that contribute to persistent caloric intake beyond homeostatic need even in the face of negative consequences. Palatable food and drugs of abuse act on many of the same motivation-related circuits in the brain, and can induce, at least superficially, similar molecular, cellular, and physiological adaptations on these circuits. As such, applying knowledge about the neurobiological mechanisms of SUDs may serve as useful heuristic to better understand the persistent overconsumption of palatable food that contributes to obesity. However, many important differences exist between the actions of drugs of abuse and palatable food in the brain. This warrants caution when attributing weight gain and obesity to the manifestation of a putative SUD-related behavioral disorder. Here, we describe similarities and differences between compulsive drug use in SUDs and overconsumption in obesity and consider the merit of the concept of "food addiction".
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Affiliation(s)
- Richard M O'Connor
- Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, United States of America
| | - Paul J Kenny
- Nash Family Department of Neuroscience, Icahn School of Medicine at Mount Sinai, United States of America.
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7
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Parsegian A, García-Fuster MJ, Hebda-Bauer E, Watson SJ, Flagel SB, Akil H. Adolescent cocaine differentially impacts psychomotor sensitization and epigenetic profiles in adult male rats with divergent affective phenotypes. Front Psychiatry 2022; 13:1024617. [PMID: 36311521 PMCID: PMC9599748 DOI: 10.3389/fpsyt.2022.1024617] [Citation(s) in RCA: 4] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/22/2022] [Accepted: 09/26/2022] [Indexed: 11/24/2022] Open
Abstract
Adolescent drug use reliably predicts increased addiction liability in adulthood, but not all individuals are equally impacted. To explore the biological bases of this differential reactivity to early life drug experience, we used a genetic rat model of temperament and evaluated the impact of adolescent cocaine exposure on adult psychomotor sensitization. Relative to adult bred low-responder (bLR) rats, bred high-responders (bHR) are more sensitive to the psychomotor-activating effects of cocaine and reinstate drug-seeking behavior more readily following prolonged cocaine exposure and/or abstinence. We found that a 7-day sensitizing cocaine regimen (15 mg/kg/day) during either adolescence or adulthood produced psychomotor sensitization in bHRs only, while a dual cocaine exposure prevented further sensitization, suggesting limits on neuroplasticity. By contrast, adolescent cocaine in bLRs shifted their resilient phenotype, rendering them more responsive to cocaine in adulthood following adolescent cocaine. To begin to explore the neural correlates of these behavioral phenotypes, we assessed two functionally opposite epigenetic chromatin modifications implicated in addiction liability, permissive acetylation (ac) and repressive tri-methylation (me3) on Histone 3 Lysine 9 (H3K9), in four striatal sub-regions. In bHRs, decreased H3K9me3 and increased acH3K9 in the nucleus accumbens (NAc) core associated with cocaine sensitization. In bLRs, the combination of cocaine exposure in adolescence and adulthood, which lead to an increased response to a cocaine challenge, also increased acH3K9 in the core. Thus, adolescent cocaine experience interacts with genetic background to elicit different behavioral profiles relevant to addiction in adulthood, with concurrent modifications in the epigenetic histone profiles in the NAc that associate with cocaine sensitization and with metaplasticity.
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Affiliation(s)
- Aram Parsegian
- Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI, United States
| | - M Julia García-Fuster
- IUNICS, University of the Balearic Islands, Palma, Spain.,Health Research Institute of the Balearic Islands (IdISBa), Palma, Spain
| | - Elaine Hebda-Bauer
- Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI, United States
| | - Stanley J Watson
- Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI, United States.,Department of Psychiatry, University of Michigan, Ann Arbor, MI, United States
| | - Shelly B Flagel
- Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI, United States.,Department of Psychiatry, University of Michigan, Ann Arbor, MI, United States
| | - Huda Akil
- Michigan Neuroscience Institute, University of Michigan, Ann Arbor, MI, United States.,Department of Psychiatry, University of Michigan, Ann Arbor, MI, United States
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8
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Blanco-Gandia MC, Montagud-Romero S, Rodríguez-Arias M. Binge eating and psychostimulant addiction. World J Psychiatry 2021; 11:517-529. [PMID: 34631457 PMCID: PMC8475000 DOI: 10.5498/wjp.v11.i9.517] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/13/2021] [Revised: 05/13/2021] [Accepted: 07/27/2021] [Indexed: 02/06/2023] Open
Abstract
Many of the various factors, characteristics, and variables involved in the addictive process can determine an individual’s vulnerability to develop drug addiction. Hedonic eating, based on pleasure rather than energy needs, modulates the same reward circuits, as do drugs of abuse. According to the last report of the World Health Organization, the worldwide obesity rate has more than doubled since 1980, reaching especially critical levels in children and young people, who are overexposed to high-fat, high-sugar, energy-dense foods. Over the past few decades, there has been an increase in the number of studies focused on how eating disorders can lead to the development of drug addiction and on the comorbidity that exists between the two disorders. Herein, we review the most recent research on the subject, focusing especially on animal models of binge eating disorders and drug addiction. The complex profile of patients with substance use and binge eating disorders requires an integrated response to dually diagnosed patients. Nutritional patterns should be considered an important variable in the treatment of substance use disorders, and future studies need to focus on specific treatments and interventions in individuals who show a special vulnerability to shift from one addiction to the other.
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Affiliation(s)
| | | | - Marta Rodríguez-Arias
- Department of Psychobiology, Facultad de Psicología, Universitat de Valencia, Valencia 46010, Spain
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9
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Abstract
As ultraprocessed foods (i.e., foods composed of mostly cheap industrial sources of dietary energy and nutrients plus additives) have become more abundant in our food supply, rates of obesity and diet-related disease have increased simultaneously. Food addiction has emerged as a phenotype of significant empirical interest within the past decade, conceptualized most commonly as a substance-based addiction to ultraprocessed foods. We detail (a) how approaches used to understand substance-use disorders may be applicable for operationalizing food addiction, (b) evidence for the reinforcing potential of ingredients in ultraprocessed foods that may drive compulsive consumptions, (c) the utility of conceptualizing food addiction as a substance-use disorder versus a behavioral addiction, and (d) clinical and policy implications that may follow if ultraprocessed foods exhibit an addictive potential. Broadly, the existing literature suggests biological and behavioral parallels between food addiction and substance addictions, with ultraprocessed foods high in both added fat and refined carbohydrates being most implicated in addictive-like eating. Future research priorities are also discussed, including the need for longitudinal studies and the potential negative impact of addictive ultraprocessed foods on children. Expected final online publication date for the Annual Review of Nutrition, Volume 41 is September 2021. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.
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Affiliation(s)
- Ashley N Gearhardt
- Department of Psychology, University of Michigan, Ann Arbor, Michigan 48109, USA;
| | - Erica M Schulte
- Department of Psychiatry, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA;
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10
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Converging vulnerability factors for compulsive food and drug use. Neuropharmacology 2021; 196:108556. [PMID: 33862029 DOI: 10.1016/j.neuropharm.2021.108556] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/29/2020] [Revised: 03/29/2021] [Accepted: 04/03/2021] [Indexed: 12/12/2022]
Abstract
Highly palatable foods and substance of abuse have intersecting neurobiological, metabolic and behavioral effects relevant for understanding vulnerability to conditions related to food (e.g., obesity, binge eating disorder) and drug (e.g., substance use disorder) misuse. Here, we review data from animal models, clinical populations and epidemiological evidence in behavioral, genetic, pathophysiologic and therapeutic domains. Results suggest that consumption of highly palatable food and drugs of abuse both impact and conversely are regulated by metabolic hormones and metabolic status. Palatable foods high in fat and/or sugar can elicit adaptation in brain reward and withdrawal circuitry akin to substances of abuse. Intake of or withdrawal from palatable food can impact behavioral sensitivity to drugs of abuse and vice versa. A robust literature suggests common substrates and roles for negative reinforcement, negative affect, negative urgency, and impulse control deficits, with both highly palatable foods and substances of abuse. Candidate genetic risk loci shared by obesity and alcohol use disorders have been identified in molecules classically associated with both metabolic and motivational functions. Finally, certain drugs may have overlapping therapeutic potential to treat obesity, diabetes, binge-related eating disorders and substance use disorders. Taken together, data are consistent with the hypotheses that compulsive food and substance use share overlapping, interacting substrates at neurobiological and metabolic levels and that motivated behavior associated with feeding or substance use might constitute vulnerability factors for one another. This article is part of the special issue on 'Vulnerabilities to Substance Abuse'.
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11
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Minhas M, Limebeer CL, Strom E, Parker LA, Leri F. High fructose corn syrup alters behavioural and neurobiological responses to oxycodone in rats. Pharmacol Biochem Behav 2021; 205:173189. [PMID: 33845083 DOI: 10.1016/j.pbb.2021.173189] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/20/2020] [Revised: 04/05/2021] [Accepted: 04/06/2021] [Indexed: 11/30/2022]
Abstract
There are indications that sugars in the diet can play a role in vulnerability to opioid abuse. The current study examined a range of neuro-behavioural interactions between oxycodone (OXY) and high fructose corn syrup (HFCS). Male Sprague-Dawley rats had access to HFCS (0 or 50%) over 26 days in their home cages and were subsequently tested on place conditioning induced by 0, 0.16 and 2.5 mg/kg OXY (3 pairings of drug and saline, each 30 min), as well as on locomotor responses to 0, 0.16 and 2.5 mg/kg OXY, and in-vivo microdialysis was employed to measure dopamine (DA) levels in the nucleus accumbens (NAc) in response to 0 and 2.5 mg/kg OXY. A complex set of interactions between HFCS exposure and responses to OXY were observed: HFCS increased place preference induced by OXY, it enhanced the suppressant effect of OXY on locomotion, and it attenuated OXY-induced elevation in DA overflow in the NAc. Taken together, these findings suggest that nutrition has the potential to influence some responses to opioids which may be relevant to their abuse.
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Affiliation(s)
- Meenu Minhas
- Department of Psychology, University of Guelph, Ontario N1G 2W1, Canada
| | - Cheryl L Limebeer
- Department of Psychology, University of Guelph, Ontario N1G 2W1, Canada
| | - Evan Strom
- Department of Psychology, University of Guelph, Ontario N1G 2W1, Canada
| | - Linda A Parker
- Department of Psychology, University of Guelph, Ontario N1G 2W1, Canada
| | - Francesco Leri
- Department of Psychology, University of Guelph, Ontario N1G 2W1, Canada.
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12
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Yamoah DA, De Man J, Onagbiye SO, Mchiza ZJ. Exposure of Children to Unhealthy Food and Beverage Advertisements in South Africa. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2021; 18:ijerph18083856. [PMID: 33916941 PMCID: PMC8067636 DOI: 10.3390/ijerph18083856] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Received: 12/21/2020] [Revised: 02/18/2021] [Accepted: 02/24/2021] [Indexed: 01/04/2023]
Abstract
Television (TV) is a powerful medium for marketing food and beverages. Food and beverage marketers tend to use this medium to target children with the hope that children will in turn influence their families' food choices. No study has assessed the compliance of TV marketers with the South African Marketing to Children pledge since the enactment of the 2014 food advertising recommendations by the South African Department of Health and the Advertising Standards Authority. This study investigated the extent and nature of advertising of unhealthy versus healthy food and beverages to children in South African TV broadcasting channels. The date, time, type, frequency and target audience of food advertisements (ads) on four free-to-air South African TV channels were recorded and captured using a structured assessment guide. The presence of persuasive marketing techniques was also assessed. Unhealthy food and beverage advertising was recorded at a significantly higher rate compared with healthy food and beverages during the time frame when children were likely to be watching TV. Brand benefit claims, health claims and power strategies (e.g., advertising using cartoon characters and celebrated individuals) were used as persuasive strategies. These persuasive strategies were used more in unhealthy versus healthy food ads. The findings are in breach of the South African Marketing to Children pledge and suggest a failure of the industry self-regulation system. We recommend the introduction of monitored and enforced statutory regulations to ensure healthy TV food advertising space.
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Affiliation(s)
- Daniel A. Yamoah
- School of Public Health, University of the Western Cape, Bellville 7535, South Africa;
| | - Jeroen De Man
- Department of Family Medicine and Population Health, University of Antwerp, 2610 Antwerp, Belgium;
| | - Sunday O. Onagbiye
- Department of Sport, Recreation and Exercise Science, University of the Western Cape, Bellville 7535, South Africa;
| | - Zandile J. Mchiza
- School of Public Health, University of the Western Cape, Bellville 7535, South Africa;
- Correspondence: ; Tel.: +27-21-959-2632
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13
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Carr KD. Modulatory Effects of Food Restriction on Brain and Behavioral Effects of Abused Drugs. Curr Pharm Des 2020; 26:2363-2371. [DOI: 10.2174/1381612826666200204141057] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/26/2019] [Accepted: 11/19/2019] [Indexed: 12/14/2022]
Abstract
Energy homeostasis is achieved, in part, by metabolic signals that regulate the incentive motivating
effects of food and its cues, thereby driving or curtailing procurement and consumption. The neural underpinnings
of these regulated incentive effects have been identified as elements within the mesolimbic dopamine pathway.
A separate line of research has shown that most drugs with abuse liability increase dopamine transmission in
this same pathway and thereby reinforce self-administration. Consequently, one might expect shifts in energy
balance and metabolic signaling to impact drug abuse risk. Basic science studies have yielded numerous examples
of drug responses altered by diet manipulation. Considering the prevalence of weight loss dieting in Western
societies, and the anorexigenic effects of many abused drugs themselves, we have focused on the CNS and behavioral
effects of food restriction in rats. Food restriction has been shown to increase the reward magnitude of diverse
drugs of abuse, and these effects have been attributed to neuroadaptations in the dopamine-innervated nucleus
accumbens. The changes induced by food restriction include synaptic incorporation of calcium-permeable
AMPA receptors and increased signaling downstream of D1 dopamine receptor stimulation. Recent studies suggest
a mechanistic model in which concurrent stimulation of D1 and GluA2-lacking AMPA receptors enables
increased stimulus-induced trafficking of GluA1/GluA2 AMPARs into the postsynaptic density, thereby increasing
the incentive effects of food, drugs, and associated cues. In addition, the established role of AMPA receptor
trafficking in enduring synaptic plasticity prompts speculation that drug use during food restriction may more
strongly ingrain behavior relative to similar use under free-feeding conditions.
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Affiliation(s)
- Kenneth D. Carr
- Departments of Psychiatry, Biochemistry and Molecular Pharmacology, New York University School of Medicine, 435 East 30th Street, New York, NY 10016, United States
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14
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Blanco-Gandía MC, Miñarro J, Rodríguez-Arias M. Common Neural Mechanisms of Palatable Food Intake and Drug Abuse: Knowledge Obtained with Animal Models. Curr Pharm Des 2020; 26:2372-2384. [DOI: 10.2174/1381612826666200213123608] [Citation(s) in RCA: 15] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/29/2019] [Accepted: 01/23/2020] [Indexed: 02/07/2023]
Abstract
Eating is necessary for survival, but it is also one of the great pleasures enjoyed by human beings.
Research to date shows that palatable food can be rewarding in a similar way to drugs of abuse, indicating
considerable comorbidity between eating disorders and substance-use disorders. Analysis of the common characteristics
of both types of disorder has led to a new wave of studies proposing a Gateway Theory of food as a vulnerability
factor that modulates the development of drug addiction. The homeostatic and hedonic mechanisms of
feeding overlap with some of the mechanisms implicated in drug abuse and their interaction plays a crucial role in
the development of drug addiction. Studies in animal models have shown how palatable food sensitizes the reward
circuit and makes individuals more sensitive to other substances of abuse, such as cocaine or alcohol. However,
when palatable food is administered continuously as a model of obesity, the consequences are different, and
studies provide controversial data. In the present review, we will cover the main homeostatic and hedonic mechanisms
that regulate palatable food intake behavior and will explain, using animal models, how different types of
diet and their intake patterns have direct consequences on the rewarding effects of psychostimulants and ethanol.
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Affiliation(s)
- Maria C. Blanco-Gandía
- Department of Psychology and Sociology, University of Zaragoza, C/ Ciudad Escolar s/n, 44003, Teruel, Spain
| | - José Miñarro
- Unit of Research Psychobiology of Drug Dependence, Department of Psychobiology, Facultad de Psicologia, Universitat de Valencia, Avda. Blasco Ibanez, 21, 46010 Valencia, Spain
| | - Marta Rodríguez-Arias
- Unit of Research Psychobiology of Drug Dependence, Department of Psychobiology, Facultad de Psicologia, Universitat de Valencia, Avda. Blasco Ibanez, 21, 46010 Valencia, Spain
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Gawliński D, Gawlińska K, Frankowska M, Filip M. Maternal Diet Influences the Reinstatement of Cocaine-Seeking Behavior and the Expression of Melanocortin-4 Receptors in Female Offspring of Rats. Nutrients 2020; 12:E1462. [PMID: 32438560 PMCID: PMC7284813 DOI: 10.3390/nu12051462] [Citation(s) in RCA: 13] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/12/2020] [Revised: 05/11/2020] [Accepted: 05/14/2020] [Indexed: 02/07/2023] Open
Abstract
Recent studies have emphasized the role of the maternal diet in the development of mental disorders in offspring. Substance use disorder is a major global health and economic burden. Therefore, the search for predisposing factors for the development of this disease can contribute to reducing the health and social damage associated with addiction. In this study, we focused on the impact of the maternal diet on changes in melanocortin-4 (MC-4) receptors as well as on behavioral changes related to cocaine addiction. Rat dams consumed a high-fat diet (HFD), high-sugar diet (HSD, rich in sucrose), or mixed diet (MD) during pregnancy and lactation. Using an intravenous cocaine self-administration model, the susceptibility of female offspring to cocaine reward and cocaine-seeking propensities was evaluated. In addition, the level of MC-4 receptors in the rat brain structures related to cocaine reward and relapse was assessed. Modified maternal diets did not affect cocaine self-administration in offspring. However, the maternal HSD enhanced cocaine-seeking behavior in female offspring. In addition, we observed that the maternal HSD and MD led to increased expression of MC-4 receptors in the nucleus accumbens, while increased MC-4 receptor levels in the dorsal striatum were observed after exposure to the maternal HSD and HFD. Taken together, it can be concluded that a maternal HSD is an important factor that triggers cocaine-seeking behavior in female offspring and the expression of MC-4 receptors.
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Affiliation(s)
| | | | | | - Małgorzata Filip
- Maj Institute of Pharmacology Polish Academy of Sciences, Department of Drug Addiction Pharmacology, Smętna Street 12, 31-343 Kraków, Poland; (D.G.); (K.G.); (M.F.)
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Gawliński D, Gawlińska K, Frankowska M, Filip M. Maternal high-sugar diet changes offspring vulnerability to reinstatement of cocaine-seeking behavior: Role of melanocortin-4 receptors. FASEB J 2020; 34:9192-9206. [PMID: 32421249 DOI: 10.1096/fj.202000163r] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/22/2020] [Revised: 04/16/2020] [Accepted: 04/21/2020] [Indexed: 12/20/2022]
Abstract
Maternal diet significantly influences the proper development of offspring in utero. Modifications of diet composition may lead to metabolic and mental disorders that may predispose offspring to a substance use disorder. We assessed the impact of a maternal high-sugar diet (HSD, rich in sucrose) consumed during pregnancy and lactation on the offspring phenotype in the context of the rewarding and motivational effects of cocaine and changes within the central melanocortin (MC) system. Using an intravenous cocaine self-administration model, we showed that maternal HSD leads to increased relapse of cocaine-seeking behavior in male offspring. In addition, we demonstrated that cocaine induces changes in the level of MC-4 receptors in the offspring brain, and these changes depend on maternal diet. These studies also reveal that an MC-4 receptor antagonist reduces the reinstatement of cocaine-seeking behavior, and offspring exposed to maternal HSD are more sensitive to its effects than offspring exposed to the maternal control diet. Taken together, the results suggest that a maternal HSD and MC-4 receptors play an important role in cocaine relapse.
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Affiliation(s)
- Dawid Gawliński
- Department of Drug Addiction Pharmacology, Maj Institute of Pharmacology Polish Academy of Sciences, Kraków, Poland
| | - Kinga Gawlińska
- Department of Drug Addiction Pharmacology, Maj Institute of Pharmacology Polish Academy of Sciences, Kraków, Poland
| | - Małgorzata Frankowska
- Department of Drug Addiction Pharmacology, Maj Institute of Pharmacology Polish Academy of Sciences, Kraków, Poland
| | - Małgorzata Filip
- Department of Drug Addiction Pharmacology, Maj Institute of Pharmacology Polish Academy of Sciences, Kraków, Poland
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The influence of opioid dependence on salt consumption and related psychological parameters in mice and humans. Drug Alcohol Depend 2019; 203:19-26. [PMID: 31400713 DOI: 10.1016/j.drugalcdep.2019.05.021] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/14/2018] [Revised: 05/22/2019] [Accepted: 05/22/2019] [Indexed: 01/15/2023]
Abstract
BACKGROUND The consumption of dietary salt (NaCl) is controlled by neuronal pathways that are modulated by endogenous opioid signalling. The latter is disrupted by chronic use of exogenous opioid receptor agonists, such as morphine. Therefore, opioid dependence may influence salt consumption, which we investigated in two complimentary studies in humans and mice. METHODS Human study: three groups were recruited: i. Individuals who are currently opioid dependent and receiving opioid substitution treatment (OST); ii. Previously opioid dependent individuals, who are currently abstinent, and; iii. Healthy controls with no history of opioid dependence. Participants tasted solutions containing different salt concentrations and indicated levels of salt 'desire', salt 'liking', and perceptions of 'saltiness'. Mouse study: preference for 0.1 M versus 0.2 M NaCl and overall levels of salt consumption were recorded during and after chronic escalating morphine treatment. RESULTS Human study: Abstinent participants' 'desire' for and 'liking' of salt was shifted towards more highly concentrated salt solutions relative to control and OST individuals. Mouse study: Mice increased their total salt consumption during morphine treatment relative to vehicle controls, which persisted for 3 days after cessation of treatment. Preference for 'low' versus 'high' concentrations of salt were unchanged. CONCLUSION These findings suggest a possible common mechanistic cross-sensitization to salt that is present in both mice and humans and builds our understanding of how opioid dependence can influence dietary salt consumption. This research may help inform better strategies to improve the diet and overall wellbeing of the growing number of individuals who develop opioid dependence.
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The impact of sugar consumption on stress driven, emotional and addictive behaviors. Neurosci Biobehav Rev 2019; 103:178-199. [DOI: 10.1016/j.neubiorev.2019.05.021] [Citation(s) in RCA: 123] [Impact Index Per Article: 20.5] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/07/2018] [Revised: 03/14/2019] [Accepted: 05/19/2019] [Indexed: 12/20/2022]
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Wiss DA, Avena N, Rada P. Sugar Addiction: From Evolution to Revolution. Front Psychiatry 2018; 9:545. [PMID: 30464748 PMCID: PMC6234835 DOI: 10.3389/fpsyt.2018.00545] [Citation(s) in RCA: 60] [Impact Index Per Article: 8.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/12/2018] [Accepted: 10/12/2018] [Indexed: 12/12/2022] Open
Abstract
The obesity epidemic has been widely publicized in the media worldwide. Investigators at all levels have been looking for factors that have contributed to the development of this epidemic. Two major theories have been proposed: (1) sedentary lifestyle and (2) variety and ease of inexpensive palatable foods. In the present review, we analyze how nutrients like sugar that are often used to make foods more appealing could also lead to habituation and even in some cases addiction thereby uniquely contributing to the obesity epidemic. We review the evolutionary aspects of feeding and how they have shaped the human brain to function in "survival mode" signaling to "eat as much as you can while you can." This leads to our present understanding of how the dopaminergic system is involved in reward and its functions in hedonistic rewards, like eating of highly palatable foods, and drug addiction. We also review how other neurotransmitters, like acetylcholine, interact in the satiation processes to counteract the dopamine system. Lastly, we analyze the important question of whether there is sufficient empirical evidence of sugar addiction, discussed within the broader context of food addiction.
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Affiliation(s)
- David A. Wiss
- Fielding School of Public Health, University of California, Los Angeles, Los Angeles, CA, United States
| | - Nicole Avena
- Icahn School of Medicine at Mount Sinai, New York, NY, United States
| | - Pedro Rada
- School of Medicine, University of Los Andes, Mérida, Venezuela
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Möller M, Fourie J, Harvey BH. Efavirenz exposure, alone and in combination with known drugs of abuse, engenders addictive-like bio-behavioural changes in rats. Sci Rep 2018; 8:12837. [PMID: 30150782 PMCID: PMC6110861 DOI: 10.1038/s41598-018-29978-3] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.9] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/04/2018] [Accepted: 07/20/2018] [Indexed: 01/09/2023] Open
Abstract
Efavirenz is abused in a cannabis-containing mixture known as Nyaope. The addictive-like effects of efavirenz (5, 10 and 20 mg/kg) was explored using conditioned place preference (CPP) in rats following sub-acute exposure vs. methamphetamine (MA; 1 mg/kg) and Δ9-tetrahydrocannabinol (THC; 0.75 mg/kg). The most addictive dose of efavirenz was then compared to THC alone and THC plus efavirenz following sub-chronic exposure using multiple behavioural measures, viz. CPP, sucrose preference test (SPT) and locomotor activity. Peripheral superoxide dismutase (SOD), regional brain lipid peroxidation and monoamines were also determined. Sub-acute efavirenz (5 mg/kg) had a significant rewarding effect in the CPP comparable to MA and THC. Sub-chronic efavirenz (5 mg/kg) and THC + efavirenz were equally rewarding using CPP, with increased cortico-striatal dopamine (DA), and increased lipid peroxidation and SOD. Sub-chronic THC did not produce CPP but significantly increased SOD and decreased hippocampal DA. Sub-chronic THC + efavirenz was hedonic in the SPT and superior to THC alone regarding cortico-striatal lipid peroxidation and sucrose preference. THC + efavirenz increased cortico-striatal DA and decreased serotonin (5-HT). Concluding, efavirenz has dose-dependent rewarding effects, increases oxidative stress and alters regional brain monoamines. Efavirenz is hedonic when combined with THC, highlighting its abuse potential when combined with THC.
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Affiliation(s)
- Marisa Möller
- Center of Excellence for Pharmaceutical Sciences, School of Pharmacy, North West University, Potchefstroom, South Africa.
| | - Jaco Fourie
- Center of Excellence for Pharmaceutical Sciences, School of Pharmacy, North West University, Potchefstroom, South Africa
| | - Brian H Harvey
- Center of Excellence for Pharmaceutical Sciences, School of Pharmacy, North West University, Potchefstroom, South Africa
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Kosheleff AR, Araki J, Hsueh J, Le A, Quizon K, Ostlund SB, Maidment NT, Murphy NP. Pattern of access determines influence of junk food diet on cue sensitivity and palatability. Appetite 2018; 123:135-145. [PMID: 29248689 PMCID: PMC5817006 DOI: 10.1016/j.appet.2017.12.009] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/01/2017] [Revised: 11/03/2017] [Accepted: 12/07/2017] [Indexed: 12/31/2022]
Abstract
AIMS Like drug addiction, cues associated with palatable foods can trigger food-seeking, even when sated. However, whether susceptibility to the motivating influence of food-related cues is a predisposing factor in overeating or a consequence of poor diet is difficult to determine in humans. Using a rodent model, we explored whether a highly palatable 'junk food' diet impacts responses to reward-paired cues in a Pavlovian-to-instrumental transfer test, using sweetened condensed milk (SCM) as the reward. The hedonic impact of SCM consumption was also assessed by analyzing licking microstructure. METHODS To probe the effects of pattern and duration of junk food exposure, we provided rats with either regular chow ad libitum (controls) or chow plus access to junk food for either 2 or 24 h per day for 1, 3, or 6 weeks. We also examined how individual susceptibility to weight gain related to these measures. RESULTS Rats provided 24 h access to the junk food diet were insensitive to the motivational effects of a SCM-paired cue when tested sated even though their hedonic experience upon reward consumption was similar to controls. In contrast, rats provided restricted, 2 h access to junk food exhibited a cue generalization phenotype under sated conditions, lever-pressing with increased vigor in response to both a SCM-paired cue, and a cue not previously paired with reward. Hedonic response was also significantly higher in these animals relative to controls. CONCLUSIONS These data demonstrate that the pattern of junk food exposure differentially alters the hedonic impact of palatable foods and susceptibility to the motivating influence of cues in the environment to promote food-seeking actions when sated, which may be consequential for understanding overeating and obesity.
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Affiliation(s)
- Alisa R Kosheleff
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA; Department of Psychology, University of California, Los Angeles, CA, USA.
| | - Jingwen Araki
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA
| | - Jennifer Hsueh
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA
| | - Andrew Le
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA
| | - Kevin Quizon
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA
| | - Sean B Ostlund
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA; Department of Anesthesiology and Perioperative Care, University of California, 3111 Gillespie Neuroscience Research Facility 837 Health Sciences Rd, Irvine, CA 92697, USA
| | - Nigel T Maidment
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA
| | - Niall P Murphy
- Hatos Center for Neuropharmacology, Department of Psychiatry and Biobehavioral Sciences, Semel Institute for Neuroscience and Human Behavior, University of California, 675 Charles E Young Dr. South, MRL #2762, Los Angeles, CA 90095, USA
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Increased ethanol consumption after interruption of fat bingeing. PLoS One 2018; 13:e0194431. [PMID: 29590149 PMCID: PMC5874030 DOI: 10.1371/journal.pone.0194431] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/27/2017] [Accepted: 03/03/2018] [Indexed: 12/21/2022] Open
Abstract
There is a marked comorbidity between alcohol abuse and eating disorders, especially in the young population. We have previously reported that bingeing on fat during adolescence increases the rewarding effects of ethanol (EtOH). The aim of the present work was to study if vulnerability to EtOH persists after cessation of binge eating. OF1 mice binged on fat (HFB: high-fat binge) during adolescence (PND 25-43) and were tested for 15 days after the last access to HFB (on PND 59) using the self-administration paradigm, the conditioned place preference (CPP) and locomotor sensitization to ethanol. Our results showed that after 15 days of cessation of fat ingestion, mice increased their consumption of ethanol and showed greater motivation to obtain ethanol. On the other hand, no effects were observed in the CPP, while an increased locomotor response to ethanol was detected. The present results confirm and extend our previous study demonstrating that the compulsive intake of fat induces long-lasting effects on the reward system that lead to an increased consumption of EtOH.
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Sweet taste liking is associated with subjective response to amphetamine in women but not men. Psychopharmacology (Berl) 2017; 234:3185-3194. [PMID: 28762072 PMCID: PMC5660927 DOI: 10.1007/s00213-017-4702-x] [Citation(s) in RCA: 16] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/01/2017] [Accepted: 07/21/2017] [Indexed: 10/19/2022]
Abstract
RATIONALE AND OBJECTIVE Preference for sweet taste rewards has been linked to the propensity for drug use in both animals and humans. Here, we tested the association between sweet taste liking and sensitivity to amphetamine reward in healthy adults. We hypothesized that sweet likers would report greater euphoria and stimulation following D-amphetamine (20 mg) compared to sweet dislikers. METHODS Men (n = 36) and women (n = 34) completed a sweet taste test in which they rated their liking of various concentrations of sucrose and filtered water (0.05, 0.10, 0.21, 0.42, and 0.83 M). Participants who preferred the highest concentration were classified as "sweet likers." All others were classified as "sweet dislikers." They then completed four sessions in which they received D-amphetamine (20 mg) and placebo in alternating order, providing self-report measures of euphoria and stimulation on the Addiction Research Center Inventory (ARCI) at regular intervals. We conducted linear mixed effects models to examine relationships between sweet liking and drug-induced euphoria and stimulation. RESULTS Sweet likers reported significantly greater amphetamine-induced euphoria than did sweet dislikers among women. By contrast, sweet liking was not associated with amphetamine response in men. No associations with stimulation were observed. CONCLUSION The association between sweet preference and amphetamine response in women is consistent with animal studies linking sweet taste preference and drug reward and also fits with observations that individuals who use drugs show a preference for sweet tastes. Whether the sex difference is related to circulating hormones, or other variables, remains to be determined.
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Blanco-Gandía MC, Aracil-Fernández A, Montagud-Romero S, Aguilar MA, Manzanares J, Miñarro J, Rodríguez-Arias M. Changes in gene expression and sensitivity of cocaine reward produced by a continuous fat diet. Psychopharmacology (Berl) 2017; 234:2337-2352. [PMID: 28456841 DOI: 10.1007/s00213-017-4630-9] [Citation(s) in RCA: 19] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/26/2017] [Accepted: 04/03/2017] [Indexed: 12/17/2022]
Abstract
RATIONALE Preclinical studies report that free access to a high-fat diet (HFD) alters the response to psychostimulants. OBJECTIVES The aim of the present study was to examine how HFD exposure during adolescence modifies cocaine effects. Gene expression of CB1 and mu-opioid receptors (MOr) in the nucleus accumbens (N Acc) and prefrontal cortex (PFC) and ghrelin receptor (GHSR) in the ventral tegmental area (VTA) were assessed. METHODS Mice were allowed continuous access to fat from PND 29, and the locomotor (10 mg/kg) and reinforcing effects of cocaine (1 and 6 mg/kg) on conditioned place preference (CPP) were evaluated on PND 69. Another group of mice was exposed to a standard diet until the day of post-conditioning, on which free access to the HFD began. RESULTS HFD induced an increase of MOr gene expression in the N Acc, but decreased CB1 receptor in the N Acc and PFC. After fat withdrawal, the reduction of CB1 receptor in the N Acc was maintained. Gene expression of GHSR in the VTA decreased during the HFD and increased after withdrawal. Following fat discontinuation, mice exhibited increased anxiety, augmented locomotor response to cocaine, and developed CPP for 1 mg/kg cocaine. HFD reduced the number of sessions required to extinguish the preference and decreased sensitivity to drug priming-induced reinstatement. CONCLUSION Our results suggest that consumption of a HFD during adolescence induces neurobiochemical changes that increased sensitivity to cocaine when fat is withdrawn, acting as an alternative reward.
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Affiliation(s)
- M Carmen Blanco-Gandía
- Departamento de Psicobiología, Facultad de Psicología, Unidad de Investigación Psicobiología de las Drogodependencias, , Universitat de València, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain
| | | | - Sandra Montagud-Romero
- Departamento de Psicobiología, Facultad de Psicología, Unidad de Investigación Psicobiología de las Drogodependencias, , Universitat de València, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain
| | - Maria A Aguilar
- Departamento de Psicobiología, Facultad de Psicología, Unidad de Investigación Psicobiología de las Drogodependencias, , Universitat de València, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain
| | - Jorge Manzanares
- Instituto de Neurociencias, Universidad Miguel Hernández-CSIC, Alicante, Spain
| | - José Miñarro
- Departamento de Psicobiología, Facultad de Psicología, Unidad de Investigación Psicobiología de las Drogodependencias, , Universitat de València, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain
| | - Marta Rodríguez-Arias
- Departamento de Psicobiología, Facultad de Psicología, Unidad de Investigación Psicobiología de las Drogodependencias, , Universitat de València, Avda. Blasco Ibáñez, 21, 46010, Valencia, Spain.
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Dorofeikova MV, Egorov AY, Filatova EV, Orlov AA. Sucrose-enriched diet during maturation increases ethanol preference in rats. DOKLADY BIOLOGICAL SCIENCES : PROCEEDINGS OF THE ACADEMY OF SCIENCES OF THE USSR, BIOLOGICAL SCIENCES SECTIONS 2017; 475:148-150. [PMID: 28861882 DOI: 10.1134/s0012496617040068] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 04/06/2017] [Indexed: 06/07/2023]
Abstract
In the present study we used a diet enriched with 10% sucrose, which was consumed by adolescent animals of the experimental group for one month. We found that consumption of sweet food during sexual maturation affected alcohol preference, anxiety, and locomotor and exploratory activity in the adult rats. Our data show that easily available tasty food during adolescence probably impairs the reward system and serves as a trigger of future alcohol preference.
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Affiliation(s)
- M V Dorofeikova
- Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia.
| | - A Yu Egorov
- Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia
- St. Petersburg State University, St. Petersburg, Russia
- Mechnikov Northwestern State Medical University, St. Petersburg, Russia
| | - E V Filatova
- Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia
| | - A A Orlov
- Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Academy of Sciences, St. Petersburg, Russia
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García-Fuster MJ, Parsegian A, Watson SJ, Akil H, Flagel SB. Adolescent cocaine exposure enhances goal-tracking behavior and impairs hippocampal cell genesis selectively in adult bred low-responder rats. Psychopharmacology (Berl) 2017; 234:1293-1305. [PMID: 28210781 PMCID: PMC5792824 DOI: 10.1007/s00213-017-4566-0] [Citation(s) in RCA: 23] [Impact Index Per Article: 2.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/27/2016] [Accepted: 02/06/2017] [Indexed: 12/14/2022]
Abstract
RATIONALE Environmental challenges during adolescence, such as drug exposure, can cause enduring behavioral and molecular changes that contribute to life-long maladaptive behaviors, including addiction. Selectively bred high-responder (bHR) and low-responder (bLR) rats represent a unique model for assessing the long-term impact of adolescent environmental manipulations, as they inherently differ on a number of addiction-related traits. bHR rats are considered "addiction-prone," whereas bLR rats are "addiction-resilient," at least under baseline conditions. Moreover, relative to bLRs, bHR rats are more likely to attribute incentive motivational value to reward cues, or to "sign-track." OBJECTIVES We utilized bHR and bLR rats to determine whether adolescent cocaine exposure can alter their inborn behavioral and neurobiological profiles, with a specific focus on Pavlovian conditioned approach behavior (i.e., sign- vs. goal-tracking) and hippocampal neurogenesis. METHODS bHR and bLR rats were administered cocaine (15 mg/kg) or saline for 7 days during adolescence (postnatal day, PND 33-39) and subsequently tested for Pavlovian conditioned approach behavior in adulthood (PND 62-75), wherein an illuminated lever (conditioned stimulus) was followed by the response-independent delivery of a food pellet (unconditioned stimulus). Behaviors directed toward the lever and the food cup were recorded as sign- and goal-tracking, respectively. Hippocampal cell genesis was evaluated on PND 77 by immunohistochemistry. RESULTS Adolescent cocaine exposure impaired hippocampal cell genesis (proliferation and survival) and enhanced the inherent propensity to goal-track in adult bLR, but not bHR, rats. CONCLUSIONS Adolescent cocaine exposure elicits long-lasting changes in stimulus-reward learning and enduring deficits in hippocampal neurogenesis selectively in adult bLR rats.
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Affiliation(s)
- M. Julia García-Fuster
- IUNICS/IdISPa, University of the Balearic Islands, Palma de Mallorca, Spain,Corresponding author: M. Julia García-Fuster. IUNICS/IdISPa, University of the Balearic Islands, Cra. Valldemossa km 7.5, E-07122 Palma de Mallorca, Spain. Phone: +34 971 259992. Fax: +34 971 259501.
| | - Aram Parsegian
- Molecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, USA
| | - Stanley J. Watson
- Molecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, USA,Department of Psychiatry, University of Michigan, Ann Arbor, USA
| | - Huda Akil
- Molecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, USA,Department of Psychiatry, University of Michigan, Ann Arbor, USA
| | - Shelly B. Flagel
- Molecular & Behavioral Neuroscience Institute, University of Michigan, Ann Arbor, USA,Department of Psychiatry, University of Michigan, Ann Arbor, USA
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Dietary supplementation with fish oil prevents high fat diet-induced enhancement of sensitivity to the locomotor stimulating effects of cocaine in adolescent female rats. Drug Alcohol Depend 2016; 165:45-52. [PMID: 27242289 PMCID: PMC4939100 DOI: 10.1016/j.drugalcdep.2016.05.013] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/03/2016] [Revised: 05/13/2016] [Accepted: 05/17/2016] [Indexed: 01/03/2023]
Abstract
BACKGROUND Eating a diet high in fat can lead to obesity, chronic metabolic disease, and increased inflammation in both the central and peripheral nervous systems. Dietary supplements that are high in omega-3 polyunsaturated fatty acids can reduce or prevent these negative health consequences in rats. Eating high fat chow also increases the sensitivity of rats to behavioral effects of drugs acting on dopamine systems (e.g., cocaine), and this effect is greatest in adolescent females. METHODS The present experiment tested the hypothesis that dietary supplementation with fish oil prevents high fat chow induced increases in sensitivity to cocaine in adolescent female rats. Female Sprague-Dawley rats (post-natal day 25-27) ate standard laboratory chow (5.7% fat), high fat chow (34.4% fat), or high fat chow supplemented with fish oil (20% w/w). Cocaine dose dependently (1-17.8mg/kg) increased locomotion and induced sensitization across 6 weeks of once-weekly testing in all rats; however, these effects were greatest in rats eating high fat chow. RESULTS Dietary supplementation with fish oil prevented enhanced locomotion and sensitization in rats eating high fat chow. There were no differences in inflammatory markers in plasma or the hypothalamus among dietary conditions. CONCLUSIONS These results demonstrate that dietary supplementation with fish oil can prevent high fat diet-induced sensitization to cocaine, but they fail to support the view that these effects are due to changes in proinflammatory cytokines. These data add to a growing literature on the relationship between diet and drug abuse and extend the potential health benefits of fish oil to stimulant drug abuse prevention.
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Eating high fat chow, but not drinking sucrose or saccharin, enhances the development of sensitization to the locomotor effects of cocaine in adolescent female rats. Behav Pharmacol 2015; 26:321-5. [PMID: 25485647 DOI: 10.1097/fbp.0000000000000114] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/27/2023]
Abstract
Eating high fat chow accelerates the development of sensitization to cocaine-induced locomotion in female rats. It is not known whether consumption of sucrose or saccharin also increases sensitivity to the behavioral effects of cocaine or whether continuous (or intermittent) access to these feeding conditions is necessary to change sensitivity. Adolescent female Sprague-Dawley rats were assigned to one of seven feeding conditions from postnatal day 25 through to postnatal day 60. The rats either ate high fat (60% kcal from fat) chow and drank water or ate standard (17% kcal from fat) chow and drank either water, a 10% sucrose solution, or a 0.1% saccharin solution. The rats either had continuous access to high fat chow, sucrose, or saccharin, or had intermittent access (i.e. 2 days/week) to these substances, with access to water and standard chow on other days. As compared with standard chow, continuous (but not intermittent) access to high fat chow enhanced the development of sensitization to cocaine-induced (1-17.8 mg/kg) locomotion; drinking sucrose or saccharin (continuous or intermittent access) did not alter the development of sensitization to cocaine-induced locomotion. The impact of feeding condition on the behavioral effects of cocaine varies between sexes and across dietary composition.
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Collins GT, Chen Y, Tschumi C, Rush EL, Mensah A, Koek W, France CP. Effects of consuming a diet high in fat and/or sugar on the locomotor effects of acute and repeated cocaine in male and female C57BL/6J mice. Exp Clin Psychopharmacol 2015; 23:228-37. [PMID: 26237320 PMCID: PMC4523901 DOI: 10.1037/pha0000019] [Citation(s) in RCA: 28] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/21/2022]
Abstract
Drug abuse and obesity are serious public health problems. Dopamine plays a central role in mediating the reinforcing effects of drugs and food. Prolonged use of drugs is known to alter the function and/or sensitivity of many neurotransmitter systems, including dopamine; however, the impact of consuming foods high in fat and/or sugar is less clear. These studies characterized the locomotor effects of acute and repeated cocaine in male and female C57BL/6J mice consuming 1 of 4 diets: (a) standard chow + water; (b) standard chow + 10% sucrose solution; (c) high-fat chow + water; or (d) high-fat chow + 10% sucrose solution. The acute locomotor effects of cocaine (3.2-32.0 mg/kg) were evaluated 4 weeks after initiating dietary conditions; the effects of repeated cocaine administration were evaluated after 5, 6, 7, and 12 weeks. During acute tests, mice consuming a diet high in fat and/or sucrose exhibited greater locomotor responses to cocaine than mice consuming standard chow and water, regardless of sex. Although diet-induced enhancements persisted across repeated cocaine testing, locomotor sensitization developed more rapidly in females drinking sucrose (and consuming either standard or high-fat chow) than in females consuming standard chow and water. In addition to providing evidence that consuming a diet high in fat and/or sugar enhances abuse-related effects of cocaine in ways that might increase vulnerability to abuse cocaine, these studies identified a potentially important sex-related difference in the interaction between nutrition and cocaine effects, with the impacts of sucrose consumption being greater in females than in males.
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Affiliation(s)
- Gregory T Collins
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
| | - Yu Chen
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
| | - Chris Tschumi
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
| | - Elise L Rush
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
| | - Ayele Mensah
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
| | - Wouter Koek
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
| | - Charles P France
- Department of Pharmacology, University of Texas Health Science Center at San Antonio
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Serafine KM, Bentley TA, Kilborn DJ, Koek W, France CP. Drinking sucrose or saccharin enhances sensitivity of rats to quinpirole-induced yawning. Eur J Pharmacol 2015; 764:529-536. [PMID: 26189020 DOI: 10.1016/j.ejphar.2015.07.036] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/15/2015] [Revised: 07/14/2015] [Accepted: 07/15/2015] [Indexed: 12/31/2022]
Abstract
Diet can impact sensitivity of rats to some of the behavioral effects of drugs acting on dopamine systems. The current study tested whether continuous access to sucrose is necessary to increase yawning induced by the dopamine receptor agonist quinpirole, or if intermittent access is sufficient. These studies also tested whether sensitivity to quinpirole-induced yawning increases in rats drinking the non-caloric sweetener saccharin. Dose-response curves (0.0032-0.32 mg/kg) for quinpirole-induced yawning were determined once weekly in rats with free access to standard chow and either continuous access to water, 10% sucrose solution, or 0.1% saccharin solution, or intermittent access to sucrose or saccharin (i.e., 2 days per week with access to water on other days). Cumulative doses of quinpirole increased then decreased yawning, resulting in an inverted U-shaped dose-response curve. Continuous or intermittent access to sucrose enhanced sensitivity to quinpirole-induced yawning. Continuous, but not intermittent, access to saccharin also enhanced sensitivity to quinpirole-induced yawning. In all groups, pretreatment with the selective D3 receptor antagonist PG01037 shifted the ascending limb of the quinpirole dose-response curve to the right, while pretreatment with the selective D2 receptor antagonist L-741,626 shifted the descending limb to the right. These results suggest that even intermittent consumption of diets containing highly palatable substances (e.g. sucrose) alters sensitivity to drugs acting on dopamine systems in a manner that could be important in vulnerability to abuse drugs.
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Affiliation(s)
- Katherine M Serafine
- Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7764, San Antonio, TX 78229, USA
| | - Todd A Bentley
- Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7764, San Antonio, TX 78229, USA
| | - Dylan J Kilborn
- Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7764, San Antonio, TX 78229, USA
| | - Wouter Koek
- Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7764, San Antonio, TX 78229, USA; Department of Psychiatry, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7764, San Antonio, TX 78229, USA
| | - Charles P France
- Department of Pharmacology, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7764, San Antonio, TX 78229, USA; Department of Psychiatry, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, Mail Code 7764, San Antonio, TX 78229, USA.
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Cummings BS, Pati S, Sahin S, Scholpa NE, Monian P, Trinquero PO, Clark JK, Wagner JJ. Differential effects of cocaine exposure on the abundance of phospholipid species in rat brain and blood. Drug Alcohol Depend 2015; 152:147-56. [PMID: 25960140 PMCID: PMC4458179 DOI: 10.1016/j.drugalcdep.2015.04.009] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/11/2014] [Revised: 04/08/2015] [Accepted: 04/08/2015] [Indexed: 01/19/2023]
Abstract
BACKGROUND Lipid profiles in the blood are altered in human cocaine users, suggesting that cocaine exposure can induce lipid remodeling. METHODS Lipid changes in the brain tissues of rats sensitized to cocaine were determined through shotgun lipidomics using electrospray ionization-mass spectrometry (ESI-MS). We also performed pairwise principal component analysis (PCA) to assess cocaine-induced changes in blood lipid profiles. Alterations in the abundance of phospholipid species were correlated with behavioral changes in the magnitude of either the initial response to the drug or locomotor sensitization. RESULTS Behavioral sensitization altered the relative abundance of several phospholipid species in the hippocampus and cerebellum, measured one week following the final exposure to cocaine. In contrast, relatively few effects on phospholipids in either the dorsal or the ventral striatum were observed. PCA analysis demonstrated that cocaine altered the relative abundance of several glycerophospholipid species as compared to saline-injected controls in blood. Subsequent MS/MS analysis identified some of these lipids as phosphatidylethanolamines, phosphatidylserines and phosphatidylcholines. The relative abundance of some of these phospholipid species were well-correlated (R(2) of 0.7 or higher) with either the initial response to cocaine or locomotor sensitization. CONCLUSION Taken together, these data demonstrate that a cocaine-induced sensitization assay results in the remodeling of specific phospholipids in rat brain tissue in a region-specific manner and also alters the intensities of certain types of phospholipid species in rat blood. These results further suggest that such changes may serve as biomarkers to assess the neuroadaptations occurring following repeated exposure to cocaine.
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Affiliation(s)
- Brian S. Cummings
- Department of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens GA, 30602,Corresponding Authors: Brian S. Cummings, 336 College of Pharmacy South, University of Georgia, Athens, GA 30602, Phone: 706-542-3792, Fax: 706-542-5358, . John J. Wagner, 501 D.W. Brooks, University of Georgia, Athens, GA 30602, 706 542-6428, 706 542-3015,
| | - Sumitra Pati
- Department of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens GA, 30602
| | - Serap Sahin
- Department of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens GA, 30602,Cumhuriyet University, Faculty of Pharmacy, Department of Biochemistry, 58140 Sivas, Turkey
| | - Natalie E. Scholpa
- Department of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens GA, 30602
| | - Prashant Monian
- Department of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens GA, 30602
| | - Paul O. Trinquero
- Department of Pharmaceutical and Biomedical Sciences, University of Georgia, Athens GA, 30602
| | - Jason K. Clark
- Department of Pharmacology and Physiology, College of Veterinary Medicine, University of Georgia, Athens GA, 30602
| | - John J. Wagner
- Department of Pharmacology and Physiology, College of Veterinary Medicine, University of Georgia, Athens GA, 30602,Corresponding Authors: Brian S. Cummings, 336 College of Pharmacy South, University of Georgia, Athens, GA 30602, Phone: 706-542-3792, Fax: 706-542-5358, . John J. Wagner, 501 D.W. Brooks, University of Georgia, Athens, GA 30602, 706 542-6428, 706 542-3015,
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Lardeux S, Kim JJ, Nicola SM. Intermittent-access binge consumption of sweet high-fat liquid does not require opioid or dopamine receptors in the nucleus accumbens. Behav Brain Res 2015; 292:194-208. [PMID: 26097003 DOI: 10.1016/j.bbr.2015.06.015] [Citation(s) in RCA: 16] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/07/2015] [Revised: 06/04/2015] [Accepted: 06/07/2015] [Indexed: 12/31/2022]
Abstract
Binge eating disorders are characterized by episodes of intense consumption of high-calorie food. In recently developed animal models of binge eating, rats given intermittent access to such food escalate their consumption over time. Consumption of calorie-dense food is associated with neurochemical changes in the nucleus accumbens, including dopamine release and alterations in dopamine and opioid receptor expression. Therefore, we hypothesized that binge-like consumption on intermittent access schedules is dependent on opioid and/or dopamine neurotransmission in the accumbens. To test this hypothesis, we asked whether injection of dopamine and opioid receptor antagonists into the core and shell of the accumbens reduced consumption of a sweet high-fat liquid in rats with and without a history of intermittent binge access to the liquid. Although injection of a μ opioid agonist increased consumption, none of the antagonists (including μ opioid, δ opioid, κ opioid, D1 dopamine and D2 dopamine receptor antagonists, as well as the broad-spectrum opioid receptor antagonist naltrexone) reduced consumption, and this was the case whether or not the animals had a prior history of intermittent access. These results suggest that consumption of sweet, fatty food does not require opioid or dopamine receptor activation in the accumbens even under intermittent access conditions that resemble human binge episodes.
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Affiliation(s)
- Sylvie Lardeux
- Department of Psychiatry, Albert Einstein College of Medicine, Bronx, NY 10461, United States
| | - James J Kim
- Department of Psychiatry, Albert Einstein College of Medicine, Bronx, NY 10461, United States
| | - Saleem M Nicola
- Department of Psychiatry, Albert Einstein College of Medicine, Bronx, NY 10461, United States; Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, United States.
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Differences in bingeing behavior and cocaine reward following intermittent access to sucrose, glucose or fructose solutions. Neuroscience 2015; 301:213-20. [PMID: 26079112 DOI: 10.1016/j.neuroscience.2015.06.015] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/24/2014] [Revised: 06/01/2015] [Accepted: 06/08/2015] [Indexed: 01/28/2023]
Abstract
Daily intermittent access to sugar solutions results in intense bouts of sugar intake (i.e. bingeing) in rats. Bingeing on sucrose, a disaccharide of glucose and fructose, has been associated with a "primed" mesolimbic dopamine (DA) pathway. Recent studies suggest glucose and fructose engage brain reward and energy-sensing mechanisms in opposing ways and may drive sucrose intake through unique neuronal circuits. Here, we examined in male Sprague-Dawley rats whether or not (1) intermittent access to isocaloric solutions of sucrose, glucose or fructose results in distinctive sugar-bingeing profiles and (2) previous sugar bingeing alters cocaine locomotor activation and/or reward, as determined by conditioned place preference (CPP). To encourage bingeing, rats were given 24-h access to water and 12-h-intermittent access to chow plus an intermittent bottle that contained water (control) or 8% solutions of sucrose, glucose or fructose for 9days, followed by ad libitum chow diet and a 10-day cocaine (15mg/kg; i.p.) CPP paradigm. By day 4 of the sugar-bingeing diet, sugar bingeing in the fructose group surpassed the glucose group, with the sucrose group being intermediate. All three sugar groups had similar chow and water intake throughout the diet. In contrast, controls exhibited chow bingeing by day 5 without altering water intake. Similar magnitudes of cocaine CPP were observed in rats with a history of sucrose, fructose or chow (control) bingeing. Notably, the glucose-bingeing rats did not demonstrate a significant cocaine CPP despite showing similar cocaine-induced locomotor activity as the other diet groups. Overall, these results show that fructose and glucose, the monosaccharide components of sucrose, produce divergent degrees of bingeing and cocaine reward.
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Hurt RT, Edakkanambeth Varayil J, Mundi MS, Martindale RG, Ebbert JO. Designation of obesity as a disease: lessons learned from alcohol and tobacco. Curr Gastroenterol Rep 2015; 16:415. [PMID: 25277042 DOI: 10.1007/s11894-014-0415-z] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/17/2022]
Abstract
Obesity is a leading cause of preventable death in the USA. The American Medical Association recently recognized obesity as meeting the definition of a chronic disease. This declaration had the intention of improving screening and long-term treatment and is historically similar to the designation of tobacco and alcohol dependence as a chronic disease. Nevertheless, it has ignited a nationwide debate in both academia and public opinion. The current article reviews the implications of treating obesity as a chronic disease, comparing the similarities in pathophysiology of obesity and other addictions, and discusses the pros and cons of this designation as it pertains to health care workers and patients.
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Affiliation(s)
- Ryan T Hurt
- Division of General Internal Medicine, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA,
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Nesil T, Kanit L, Pogun S. Bitter taste and nicotine preference: evidence for sex differences in rats. THE AMERICAN JOURNAL OF DRUG AND ALCOHOL ABUSE 2014; 41:57-67. [DOI: 10.3109/00952990.2014.990091] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/13/2022]
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Blum K, Thanos PK, Gold MS. Dopamine and glucose, obesity, and reward deficiency syndrome. Front Psychol 2014; 5:919. [PMID: 25278909 PMCID: PMC4166230 DOI: 10.3389/fpsyg.2014.00919] [Citation(s) in RCA: 127] [Impact Index Per Article: 11.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/02/2014] [Accepted: 08/01/2014] [Indexed: 01/08/2023] Open
Abstract
Obesity as a result of overeating as well as a number of well described eating disorders has been accurately considered to be a world-wide epidemic. Recently a number of theories backed by a plethora of scientifically sound neurochemical and genetic studies provide strong evidence that food addiction is similar to psychoactive drug addiction. Our laboratory has published on the concept known as Reward Deficiency Syndrome (RDS) which is a genetic and epigenetic phenomena leading to impairment of the brain reward circuitry resulting in a hypo-dopaminergic function. RDS involves the interactions of powerful neurotransmitters and results in abnormal craving behavior. A number of important facts which could help translate to potential therapeutic targets espoused in this focused review include: (1) consumption of alcohol in large quantities or carbohydrates binging stimulates the brain’s production of and utilization of dopamine; (2) in the meso-limbic system the enkephalinergic neurons are in close proximity, to glucose receptors; (3) highly concentrated glucose activates the calcium channel to stimulate dopamine release from P12 cells; (4) a significant correlation between blood glucose and cerebrospinal fluid concentrations of homovanillic acid the dopamine metabolite; (5) 2-deoxyglucose (2DG), the glucose analog, in pharmacological doses is associated with enhanced dopamine turnover and causes acute glucoprivation. Evidence from animal studies and fMRI in humans support the hypothesis that multiple, but similar brain circuits are disrupted in obesity and drug dependence and for the most part, implicate the involvement of DA-modulated reward circuits in pathologic eating behaviors. Based on a consensus of neuroscience research treatment of both glucose and drug like cocaine, opiates should incorporate dopamine agonist therapy in contrast to current theories and practices that utilizes dopamine antagonistic therapy. Considering that up until now clinical utilization of powerful dopamine D2 agonists have failed due to chronic down regulation of D2 receptors newer targets based on novel less powerful D2 agonists that up-regulate D2 receptors seems prudent. We encourage new strategies targeted at improving DA function in the treatment and prevention of obesity a subtype of reward deficiency.
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Affiliation(s)
- Kenneth Blum
- Department of Psychiatry, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville FL, USA ; Department of Addiction Research & Therapy, Malibu Beach Recovery Center Malibu Beach, CA, USA
| | - Panayotis K Thanos
- Behavior Neuropharmacology and Neuroimaging Lab, Department of Psychology, State University of New York Stony Brook, NY, USA
| | - Mark S Gold
- Department of Psychiatry, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville FL, USA ; Department of Addiction Research & Therapy, Malibu Beach Recovery Center Malibu Beach, CA, USA
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Hone-Blanchet A, Fecteau S. Overlap of food addiction and substance use disorders definitions: analysis of animal and human studies. Neuropharmacology 2014; 85:81-90. [PMID: 24863044 DOI: 10.1016/j.neuropharm.2014.05.019] [Citation(s) in RCA: 79] [Impact Index Per Article: 7.2] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/21/2014] [Revised: 05/11/2014] [Accepted: 05/13/2014] [Indexed: 01/24/2023]
Abstract
Food has both homeostatic and hedonic components, which makes it a potent natural reward. Food related reward could therefore promote an escalation of intake and trigger symptoms associated to withdrawal, suggesting a behavioral parallel with substance abuse. Animal and human theoretical models of food reward and addiction have emerged, raising further interrogations on the validity of a bond between Substance Use Disorders, as clinically categorized in the DSM 5, and food reward. These models propose that highly palatable food items, rich in sugar and/or fat, are overly stimulating to the brain's reward pathways. Moreover, studies have also investigated the possibility of causal link between food reward and the contemporary obesity epidemic, with obesity being potentiated and maintained due to this overwhelming food reward. Although natural rewards are a hot topic in the definition and categorization of Substance Use Disorders, proofs of concept and definite evidence are still inconclusive. This review focuses on available results from experimental studies in animal and human models exploring the concept of food addiction, in an effort to determine if it depicts a specific phenotype and if there is truly a neurobiological similarity between food addiction and Substance Use Disorders. It describes results from sugar, fat and sweet-fat bingeing in rodent models, and behavioral and neurobiological assessments in different human populations. Although pieces of behavioral and neurobiological evidence supporting a food addiction phenotype in animals and humans are interesting, it seems premature to conclude on its validity.
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Affiliation(s)
- Antoine Hone-Blanchet
- Laboratory of Canada Research Chair in Cognitive Neuroscience, Centre Interdisciplinaire de Recherche en Réadaptation et Intégration Sociale, Centre de Recherche de l'Institut Universitaire en Santé Mentale de Québec, Medical School, Laval University, Canada
| | - Shirley Fecteau
- Laboratory of Canada Research Chair in Cognitive Neuroscience, Centre Interdisciplinaire de Recherche en Réadaptation et Intégration Sociale, Centre de Recherche de l'Institut Universitaire en Santé Mentale de Québec, Medical School, Laval University, Canada; Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center, Harvard Medical School, USA.
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Bell IR. Nonlinear effects of nanoparticles: biological variability from hormetic doses, small particle sizes, and dynamic adaptive interactions. Dose Response 2014; 12:202-32. [PMID: 24910581 PMCID: PMC4036395 DOI: 10.2203/dose-response.13-025.bell] [Citation(s) in RCA: 48] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/21/2022] Open
Abstract
Researchers are increasingly focused on the nanoscale level of organization where biological processes take place in living systems. Nanoparticles (NPs, e.g., 1-100 nm diameter) are small forms of natural or manufactured source material whose properties differ markedly from those of the respective bulk forms of the "same" material. Certain NPs have diagnostic and therapeutic uses; some NPs exhibit low-dose toxicity; other NPs show ability to stimulate low-dose adaptive responses (hormesis). Beyond dose, size, shape, and surface charge variations of NPs evoke nonlinear responses in complex adaptive systems. NPs acquire unique size-dependent biological, chemical, thermal, optical, electromagnetic, and atom-like quantum properties. Nanoparticles exhibit high surface adsorptive capacity for other substances, enhanced bioavailability, and ability to cross otherwise impermeable cell membranes including the blood-brain barrier. With super-potent effects, nano-forms can evoke cellular stress responses or therapeutic effects not only at lower doses than their bulk forms, but also for longer periods of time. Interactions of initial effects and compensatory systemic responses can alter the impact of NPs over time. Taken together, the data suggest the need to downshift the dose-response curve of NPs from that for bulk forms in order to identify the necessarily decreased no-observed-adverse-effect-level and hormetic dose range for nanoparticles.
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Intermittent feeding schedules--behavioural consequences and potential clinical significance. Nutrients 2014; 6:985-1002. [PMID: 24599157 PMCID: PMC3967173 DOI: 10.3390/nu6030985] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2013] [Revised: 02/06/2014] [Accepted: 02/17/2014] [Indexed: 11/26/2022] Open
Abstract
Food availability and associated sensory cues such as olfaction are known to trigger a range of hormonal and behavioural responses. When food availability is predictable these physiological and behavioural responses can become entrained to set times and occur in anticipation of food rather than being dependent on the food-related cues. Here we summarise the range of physiological and behavioural responses to food when the time of its availability is unpredictable, and consider the potential to manipulate feeding patterns for benefit in metabolic and mental health.
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Keralapurath MM, Clark JK, Hammond S, Wagner JJ. Cocaine- or stress-induced metaplasticity of LTP in the dorsal and ventral hippocampus. Hippocampus 2014; 24:577-90. [PMID: 24464838 DOI: 10.1002/hipo.22250] [Citation(s) in RCA: 30] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 01/18/2014] [Indexed: 01/04/2023]
Abstract
Despite the well documented role of the hippocampus in various modes of drug reinstatement behavior, the persisting effects of in vivo cocaine exposure on hippocampal synaptic plasticity are not sufficiently understood. In this report we investigated the effects of cocaine conditioning on long-term potentiation (LTP) in the CA1 region of hippocampus along its septotemporal axis. Male Sprague-Dawley rats experienced a behavioral protocol, in which locomotor activity was monitored in response to various conditioning treatments. LTP was measured in ex vivo slice preparations taken 1-2 weeks after the last behavioral session from the ventral (vH) and dorsal (dH) sectors of hippocampus. Unexpectedly, experiencing the minor intermittent stimuli of the behavioral protocol caused stress-induced metaplastic changes in both vH (increased LTP) and dH (decreased LTP) in the saline conditioned rats relative to behaviorally naïve controls. These stress effects in the vH and dH were blocked by conditioning with either mineralocorticoid (spironolactone) or glucocorticoid (mifepristone) antagonists, respectively. Stress-induced metaplasticity in the vH was also prevented by prior administration of the kappa opioid antagonist nor-binaltorphimine. Cocaine conditioning induced locomotor sensitization and significantly increased LTP in the vH without causing significant change in LTP in the dH. Cocaine-induced metaplasticity in the vH was prevented by co-administration of the dopamine D2-like antagonist eticlopride during cocaine conditioning, but not by co-administration of the D1/5 antagonist SCH 23390. Our results suggest that the functional connectivity of hippocampus is altered by metaplastic triggers such as exposure to drugs of abuse and/or stressors, thereby shifting the efferent output of hippocampus from dH (cortical) toward vH (limbic) influenced circuits.
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Affiliation(s)
- Madhusudhanan M Keralapurath
- Department of Physiology and Pharmacology, University of Georgia, Athens, Georgia; Interdisciplinary Toxicology Program, University of Georgia, Athens, Georgia
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Davis C. From passive overeating to "food addiction": a spectrum of compulsion and severity. ISRN OBESITY 2013; 2013:435027. [PMID: 24555143 PMCID: PMC3901973 DOI: 10.1155/2013/435027] [Citation(s) in RCA: 73] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 03/20/2013] [Accepted: 04/16/2013] [Indexed: 01/17/2023]
Abstract
A psychobiological dimension of eating behaviour is proposed, which is anchored at the low end by energy intake that is relatively well matched to energy output and is reflected by a stable body mass index (BMI) in the healthy range. Further along the continuum are increasing degrees of overeating (and BMI) characterized by more severe and more compulsive ingestive behaviours. In light of the many similarities between chronic binge eating and drug abuse, several authorities have adopted the perspective that an apparent dependence on highly palatable food-accompanied by emotional and social distress-can be best conceptualized as an addiction disorder. Therefore, this review also considers the overlapping symptoms and characteristics of binge eating disorder (BED) and models of food addiction, both in preclinical animal studies and in human research. It also presents this work in the context of the modern and "toxic" food environment and therein the ubiquitous triggers for over-consumption. We complete the review by providing evidence that what we have come to call "food addiction" may simply be a more acute and pathologically dense form of BED.
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Affiliation(s)
- Caroline Davis
- Kinesiology & Health Sciences, Faculty of Health, York University, 343 Bethune College, 4700 Keele Street, Toronto, ON, Canada M3J 1P3
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Zhang C, Tallarida CS, Raffa RB, Rawls SM. Sucrose produces withdrawal and dopamine-sensitive reinforcing effects in planarians. Physiol Behav 2013; 112-113:8-13. [PMID: 23415661 DOI: 10.1016/j.physbeh.2013.02.002] [Citation(s) in RCA: 17] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/13/2012] [Revised: 11/13/2012] [Accepted: 02/08/2013] [Indexed: 11/15/2022]
Abstract
Sucrose produces physical dependence and reinforcing effects in rats. We hypothesized that similar effects could be demonstrated in planarians, the earliest animal with a centralized nervous system. We used two assays, one that quantifies withdrawal responses during drug absence as a reduction in motility and another that quantifies reinforcing effects using a conditioned place preference (CPP) design. In withdrawal experiments, planarians exposed to sucrose (1%) for 60 min and then tested in water for 5 min displayed reduced motility compared to water controls. Acute or continuous sucrose (1%) exposure did not affect motility. CPP experiments used a biased design to capitalize upon planarians' natural preference for the dark (pretest, sucrose conditioning in the light, posttest). Planarians conditioned with sucrose (1%) displayed a greater preference shift than sucrose-naïve planarians. Glucose (0.1, 1%), but not the non-digestible disaccharide lactulose (0.1, 1%), also produced a greater preference shift than water-exposed planarians. Development of sucrose-induced CPP was inhibited when sucrose (1%) conditioning was conducted in combination with dopamine receptor antagonists SCH 23390 (1 μM) or sulpiride (1 μM). These results suggest that the rewarding and reinforcing effects of sugar are highly conserved across species and that planarians offer an invertebrate model to provide insight into the pharmacological effects of sucrose and related sweeteners.
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Affiliation(s)
- Charlie Zhang
- Department of Pharmacology, Temple University School of Medicine, Philadelphia, PA 19140, USA
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Hammond S, Seymour CM, Burger A, Wagner JJ. D-Serine facilitates the effectiveness of extinction to reduce drug-primed reinstatement of cocaine-induced conditioned place preference. Neuropharmacology 2013; 64:464-71. [PMID: 22728761 PMCID: PMC3445779 DOI: 10.1016/j.neuropharm.2012.06.022] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/31/2012] [Revised: 06/01/2012] [Accepted: 06/11/2012] [Indexed: 01/02/2023]
Abstract
Addiction is a disease that is characterized by compulsive drug-seeking and use despite negative health and social consequences. One obstacle in treating addiction is a high susceptibility for relapse which persists despite prolonged periods of abstinence. Relapse can be triggered by drug predictive stimuli such as environmental context and drug associated cues, as well as the addictive drug itself. The conditioned place preference (CPP) behavioral model is a useful paradigm for studying the ability of these drug predictive stimuli to reinstate drug-seeking behavior. The present study investigated the dose-dependent effects of D-serine (10 mg/kg, 30 mg/kg and 100 mg/kg) on extinction training and drug-primed reinstatement in cocaine-conditioned rats. In the first experiment, D-serine had no effect on the acquisition or development of cocaine-induced locomotor sensitization or CPP. In the second experiment, D-serine treatment resulted in significantly decreased time spent in the drug-paired compartment following completion of an extinction protocol. A cocaine-primed reinstatement test indicated that the combination of extinction training along with D-serine treatment resulted in a significant reduction of drug-seeking behavior. The third experiment assessed D-serine's long-term effects to diminish drug-primed reinstatement. D-serine treatment given during extinction was effective in reducing drug-seeking for more than four weeks of abstinence after the last cocaine exposure. These findings demonstrate that D-serine may be an effective adjunct therapeutic agent along with cognitive behavioral therapy for the treatment of cocaine addiction. This article is part of a Special Issue entitled 'Cognitive Enhancers'.
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Affiliation(s)
- Sherri Hammond
- Department of Physiology & Pharmacology, University of Georgia, Athens, USA
- Neuroscience Program, University of Georgia, Athens, USA
| | - Claire M. Seymour
- Department of Physiology & Pharmacology, University of Georgia, Athens, USA
| | - Ashley Burger
- Department of Physiology & Pharmacology, University of Georgia, Athens, USA
| | - John J. Wagner
- Department of Physiology & Pharmacology, University of Georgia, Athens, USA
- Neuroscience Program, University of Georgia, Athens, USA
- Interdisciplinary Toxicology Program, University of Georgia, Athens, USA
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Stice E, Figlewicz DP, Gosnell BA, Levine AS, Pratt WE. The contribution of brain reward circuits to the obesity epidemic. Neurosci Biobehav Rev 2012; 37:2047-58. [PMID: 23237885 DOI: 10.1016/j.neubiorev.2012.12.001] [Citation(s) in RCA: 181] [Impact Index Per Article: 13.9] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/04/2012] [Revised: 11/21/2012] [Accepted: 12/03/2012] [Indexed: 12/22/2022]
Abstract
One of the defining characteristics of the research of Ann E. Kelley was her recognition that the neuroscience underlying basic learning and motivation processes also shed significant light upon mechanisms underlying drug addiction and maladaptive eating patterns. In this review, we examine the parallels that exist in the neural pathways that process both food and drug reward, as determined by recent studies in animal models and human neuroimaging experiments. We discuss contemporary research that suggests that hyperphagia leading to obesity is associated with substantial neurochemical changes in the brain. These findings verify the relevance of reward pathways for promoting consumption of palatable, calorically dense foods, and lead to the important question of whether changes in reward circuitry in response to intake of such foods serve a causal role in the development and maintenance of some cases of obesity. Finally, we discuss the potential value for future studies at the intersection of the obesity epidemic and the neuroscience of motivation, as well as the potential concerns that arise from viewing excessive food intake as an "addiction". We suggest that it might be more useful to focus on overeating that results in frank obesity, and multiple health, interpersonal, and occupational negative consequences as a form of food "abuse".
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Affiliation(s)
- Eric Stice
- Oregon Research Institute, 1776 Millrace Drive, Eugene, OR 97403, United States.
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Abstract
The evidence for food's addictive properties is steadily growing. In addition to clinical and evolutionary plausibility, the possibility of addiction to food is supported by animal model research and increasingly by research with humans. Much as classic drugs of abuse "hijack" the brain, accumulating evidence with food suggests a similar impact, but with weaker effects. Although neurobiological evidence for food addiction is compelling, dependence as conceptualized with respect to alcohol and other drugs of abuse is fundamentally a behavioral disorder. Thus, we review the current state of food addiction research in the context of each of the diagnostic criterion for dependence (ie, tolerance, withdrawal, loss of control) and briefly explore other relevant addiction topics such as expectancies, reinforcement, and incentive salience. There is substantial evidence that some people lose control over their food consumption, suffer from repeated failed attempts to reduce their intake, and are unable to abstain from certain types of food or reduce consumption in the face of negative consequences. Although there is some evidence for other dependence criterion, further research is needed to examine tolerance and withdrawal to high-fat sweets, time spent in obtaining, using, and recovering from excess food consumption and the degree to which important activities are given up due to overconsumption. As science continues forward and both the public and elected leaders become aware that food may trigger an addictive process, this information will likely be used to inform policy. Thus, researchers need to carefully consider the implications of their work and the way in which the results may be interpreted.
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Bell IR, Howerter A, Jackson N, Brooks AJ, Schwartz GE. Multiweek resting EEG cordance change patterns from repeated olfactory activation with two constitutionally salient homeopathic remedies in healthy young adults. J Altern Complement Med 2012; 18:445-53. [PMID: 22594648 DOI: 10.1089/acm.2011.0931] [Citation(s) in RCA: 13] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/18/2023] Open
Abstract
OBJECTIVES Electroencephalography (EEG) offers psychophysiologic tools to improve sensitivity for detecting objective effects in complementary and alternative medicine. This current investigation extended prior clinical research studies to evaluate effects of one of two different homeopathic remedies on resting EEG cordance after an olfactory activation protocol on healthy young adults with remedy-relevant, self-perceived characteristics. METHODS Ninety-seven (7) young adults (N=97, mean age 19 years, 55% women) with good self-rated global health and screened for homeopathic constitutional types consistent with one of two remedies (either Sulphur or Pulsatilla) underwent three weekly laboratory sessions. At each visit, subjects had 5-minute resting, eyes-closed EEG recordings before and after a placebo-controlled olfactory activation task with their constitutionally relevant verum remedy. One remedy potency (6c, 12c, or 30c) used per week, was presented in a randomized order over the 3 sessions. Prefrontal resting EEG cordance values at Fp1 and Fp2 were computed from artifact-free 2-minute EEG samples from the presniffing and postsniffing rest periods. Cordance derives from an algorithm that incorporates absolute and relative EEG values. RESULTS The data showed significant two-way oscillatory interactions of remedy by time for ß, α, θ, and δ cordance, controlling for gender and chemical sensitivity. CONCLUSIONS EEG cordance provided a minimally invasive technique for assessing objective nonlinear physiologic effects of two different homeopathic remedies salient to the individuals who received them. Time factors modulated the direction of effects. Given previous evidence of correlations between cordance and single-photon emission computed tomography, these findings encourage additional neuroimaging research on nonlinear psychophysiologic effects of specific homeopathic remedies.
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Affiliation(s)
- Iris R Bell
- Department of Family & Community Medicine, The University of Arizona, College of Medicine, Tucson, AZ 85719, USA.
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Ahn S, Phillips AG. Repeated cycles of restricted food intake and binge feeding disrupt sensory-specific satiety in the rat. Behav Brain Res 2012; 231:279-85. [DOI: 10.1016/j.bbr.2012.02.017] [Citation(s) in RCA: 21] [Impact Index Per Article: 1.6] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/02/2011] [Revised: 02/03/2012] [Accepted: 02/08/2012] [Indexed: 01/04/2023]
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Alsiö J, Olszewski PK, Levine AS, Schiöth HB. Feed-forward mechanisms: addiction-like behavioral and molecular adaptations in overeating. Front Neuroendocrinol 2012; 33:127-39. [PMID: 22305720 DOI: 10.1016/j.yfrne.2012.01.002] [Citation(s) in RCA: 58] [Impact Index Per Article: 4.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/21/2011] [Revised: 11/24/2011] [Accepted: 01/13/2012] [Indexed: 12/23/2022]
Abstract
Food reward, not hunger, is the main driving force behind eating in the modern obesogenic environment. Palatable foods, generally calorie-dense and rich in sugar/fat, are thus readily overconsumed despite the resulting health consequences. Important advances have been made to explain mechanisms underlying excessive consumption as an immediate response to presentation of rewarding tastants. However, our understanding of long-term neural adaptations to food reward that oftentimes persist during even a prolonged absence of palatable food and contribute to the reinstatement of compulsive overeating of high-fat high-sugar diets, is much more limited. Here we discuss the evidence from animal and human studies for neural and molecular adaptations in both homeostatic and non-homeostatic appetite regulation that may underlie the formation of a "feed-forward" system, sensitive to palatable food and propelling the individual from a basic preference for palatable diets to food craving and compulsive, addiction-like eating behavior.
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Affiliation(s)
- Johan Alsiö
- Department of Neuroscience, Functional Pharmacology, Uppsala University, Biomedical Center, Box 593, SE-751 24 Uppsala, Sweden.
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Baladi MG, Daws LC, France CP. You are what you eat: influence of type and amount of food consumed on central dopamine systems and the behavioral effects of direct- and indirect-acting dopamine receptor agonists. Neuropharmacology 2012; 63:76-86. [PMID: 22710441 DOI: 10.1016/j.neuropharm.2012.02.005] [Citation(s) in RCA: 34] [Impact Index Per Article: 2.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/07/2011] [Revised: 12/21/2011] [Accepted: 02/07/2012] [Indexed: 12/27/2022]
Abstract
The important role of dopamine (DA) in mediating feeding behavior and the positive reinforcing effects of some drugs is well recognized. Less widely studied is how feeding conditions might impact the sensitivity of drugs acting on DA systems. Food restriction, for example, has often been the focus of aging and longevity studies; however, other studies have demonstrated that mild food restriction markedly increases sensitivity to direct- and indirect-acting DA receptor agonists. Moreover, it is becoming clear that not only the amount of food, but the type of food, is an important factor in modifying the effects of drugs. Given the increased consumption of high fat and sugary foods, studies are exploring how consumption of highly palatable food impacts DA neurochemistry and the effects of drugs acting on these systems. For example, eating high fat chow increases sensitivity to some behavioral effects of direct- as well as indirect-acting DA receptor agonists. A compelling mechanistic possibility is that central DA pathways that mediate the effects of some drugs are regulated by one or more of the endocrine hormones (e.g. insulin) that undergo marked changes during food restriction or after consuming high fat or sugary foods. Although traditionally recognized as an important signaling molecule in regulating energy homeostasis, insulin can also regulate DA neurochemistry. Because direct- and indirect-acting DA receptor drugs are used therapeutically and some are abused, a better understanding of how food intake impacts response to these drugs would likely facilitate improved treatment of clinical disorders and provide information that would be relevant to the causes of vulnerability to abuse drugs. This article is part of a Special Issue entitled 'Central Control of Food Intake'.
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Affiliation(s)
- Michelle G Baladi
- Department of Pharmacology, University of Texas Health Science Center at San Antonio, San Antonio, TX, USA
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