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Copyright ©2010 Baishideng Publishing Group Co.
World J Biol Chem. May 26, 2010; 1(5): 95-102
Published online May 26, 2010. doi: 10.4331/wjbc.v1.i5.95
Figure 4
Figure 4 Metabotropic glutamate receptor currents are reduced in PNs from PMCA2-/- mice. Given the interaction between metabotropic glutamate receptors (mGluR1) and PMCA2[24] we tested mGluR1 function using an electrophysiological assay. A: Representative traces of mGluR1 dependent inward currents in response to increasing numbers of 100 Hz stimulation to the PFs[36]. The timing of the stimulation is shown by the vertical arrows. As the number of stimulations increased, the amplitude of the evoked inward current increased, as is evident in the wild type PMCA2+/+ example. In the wild type, the responses to 0, 3, 5, 7 and 9 stimuli are shown for a single cell and for the PMCA2-/- cell the responses to 0, 3, 5, 7, 8 and 9 stimuli are shown. The responses from PMCA2-/- PNs were much reduced both in size and peak response; note the smaller vertical amplitude scale bar in the lower panel. These recordings were made with other ionotropic excitatory and inhibitory synaptic events, pharmacologically blocked, and also in the presence of TBOA to enhance available glutamate by preventing its uptake[26]; as expected the inward currents were abolished by the application of the mGluR1 antagonist, 10 μmol/L CPPCOEt, n = 6. mGluR currents were unaffected by the application of the PMCA inhibitor 10 μmol/L carboxyeosin, n = 3, P = 0.6 paired t-test, data not shown; B: The combined mean data where the increase in the amplitude of the mGluR current in wild type PMCA2+/+ PNs is evident as the number of stimuli increased. Values are mean and error bars are SE, error bars are within the size of the open symbols in the case of the PMCA2-/- data.