Metabotropic glutamate receptor enhancement of spontaneous IPSCs in neocortical interneurons Fu-Ming Zhou and John J. Hablitz Department of Neurobiology, University of Alabama at Birmingham, Birmingham, AL 35294, USA
APStracts 4:109N, 1997.
ABSTRACT
Using neocortical layer I neurons as a model for GABAergic interneurons, we have studied GABAA receptor mediated spontaneous IPSCs and modulation by metabotropic glutamate receptors (mGluRs). In the presence of 0.5 M TTX and ionotropic glutamate receptor antagonists and under symmetrical Cl- conditions, the mean amplitude of miniature IPSCs (mIPSCs) was around 50 pA at a holding potential of -70 mV with individual events ranging from 10 to 400 pA. Averaged mIPSCs had a 10-90% rise time of about 0.6 ms. The decay was double exponential. The fast component had a time constant of about 4 ms and comprised about 40% of the total amplitude. The slow component had a time constant of about 22 ms. The frequency of spontaneous IPSCs sIPSCs), recorded in the absence of TTX, was increased by bath application of the mGluR agonist 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) (10-100 (M) or the group I mGluR selective agonist quisqualic acid (Quis) (0.5 to 1 (M). Under identical conditions, mIPSCs were not affected. The kinetics of sIPSCs and mIPSCs were not altered by ACPD or Quis. Quis (1 (M) induced an inward current of about 70 pA at a holding potential of -70 mV whereas ACPD (40-200 (M) induced a smaller inward current. This current was linear over the voltage range -70 mV to 30 mV and reversed polarity near 0 mV. In current clamp recordings, both Quis and ACPD induced a strong depolarization and action potential firing in layer I and deeper layer interneurons. We conclude that neocortical layer I neurons receive GABAA receptor-mediated inhibitory synaptic inputs. Activation of mGluRs, possibly mGluR1 and/or mGluR5, causes an enhancement of inhibitory synaptic transmission by directly depolarizing cortical GABAergic interneurons through the opening of nonselective cation channels. 

Received 10 April 1997; accepted in final form 20 June 1997.
APS Manuscript Number J292-7
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 15 July 1997