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J Neurophysiol 80: 1670-1677, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 80 No. 4 October 1998, pp. 1670-1677
Copyright ©1998 The American Physiological Society

Zinc and Zolpidem Modulate mIPSCs in Rat Neocortical Pyramidal Neurons

Tony Defazio and John J. Hablitz

Department of Neurobiology, University of Alabama at Birmingham, Birmingham, Alabama 35294

DeFazio, Tony and John J. Hablitz. Zinc and zolpidem modulate mIPSCs in rat neocortical pyramidal neurons. J. Neurophysiol. 80: 1670-1677, 1998. Pharmacological modulation of gamma -aminobutyric acid-A (GABAA) receptors can provide important information on the types of subunits composing these receptors. In recombinant studies, zinc more potently inhibits alpha beta subunits compared with the alpha beta gamma combination, whereas modulation by nanomolar concentrations of the benzodiazepine type 1-selective agonist zolpidem is conferred by the alpha 1beta gamma 2 subunit combination. We examined four properties of miniature inhibitory postsynaptic currents (mIPSCs) from identified necortical pyramidal cells in rat brain slices: decay time constant, peak amplitude, rate of rise, and interevent interval. Exposure to 50 µM zinc reduced the decay time constant, peak amplitude, and rate of rise with no effect on interevent interval. Zolpidem enhanced mIPSCs in a concentration-dependent manner. Both 20 and 100 nM zolpidem increased the decay time constants of mIPSCs. In some cells, both peak amplitude and rate of rise were also enhanced. All cells treated with zinc were also responsive to zolpidem. These results show that neocortical pyramidal cells have a population of GABAA receptors sensitive to both zinc and zolpidem.




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