The Journal of Neurophysiology Vol. 78 No. 5 November 1997, pp. 2287-2295
Copyright ©1997 The American Physiological Society

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, Alabama 35294

Zhou, Fu-Ming and John J. Hablitz. Metabotropic glutamate receptor enhancement of spontaneous IPSCs in neocortical interneurons. J. Neurophysiol. 78: 2287-2295, 1997. Using neocortical layer I neurons as a model for GABAergic interneurons, we have studied -aminobutyric acid-A (GABA_A) receptor-mediated spontaneous inhibitory postsynaptic currents (IPSCs) and modulation by metabotropic glutamate receptors (mGluRs). In the presence of 0.5 µM tetrodotoxin (TTX) and ionotropic glutamate receptor antagonists and under symmetrical Cl conditions, the mean amplitude of miniature IPSCs (mIPSCs) was ~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 ~0.6 ms. The decay was double exponential. The fast component had a time constant of ~4 ms and comprised ~40% of the total amplitude. The slow component had a time constant of ~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 µM) or the group I mGluR selective agonist quisqualic acid (Quis; 0.5-1 µM). Under identical conditions, mIPSCs were not affected. The kinetics of sIPSCs and mIPSCs were not altered by ACPD or Quis. Quis (1 µM) induced an inward current of ~70 pA at a holding potential of 70 mV, whereas ACPD (40-200 µM) induced a smaller inward current. This current was linear over the voltage range 70 to +30 mV and reversed polarity near 0 mV. In current-clamp recordings, both Quis and ACPD induced a depolarization and action potential firing in layer I and deeper layer interneurons. We conclude that neocortical layer I neurons receive GABA_A receptor-mediated inhibitory synaptic inputs. Activation of mGluRs, possibly mGluR1 and/or mGluR5, causes an enhancement of inhibitory synaptic transmission by directly depolarizing corticalGABAergic interneurons through the opening of nonselective cation channels.

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