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The Journal of Neuroscience, July 1, 1998, 18(13):4870-4882
Evidence for Metabotropic Glutamate Receptor Activation in the Induction of Depolarization-Induced Suppression of Inhibition in Hippocampal CA1
Wade Morishita, Sergei A. Kirov, and Bradley E. Alger Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201
Depolarization-induced suppression of inhibition (DSI) is a transient reduction of GABAA receptor-mediated IPSCs that is mediated by a retrograde signal from principal cells to interneurons. Using whole-cell recordings, we tested the hypothesis that mGluRs are involved in the DSI process in hippocampal CA1, as has been proposed for cerebellar DSI. Group II mGluR agonists failed to affect either evoked monosynaptic IPSCs or DSI, and forskolin, which blocks cerebellar DSI, did not affect CA1 DSI. Group I and group III mGluR agonists reduced IPSCs, but only group I agonists occluded DSI. (S)-MCPG blocked (1S,3R)-ACPD-induced IPSC suppression and markedly reduced DSI, whereas group III antagonists had no effect on DSI. Many other similarities between DSI and the (1S,3R)-ACPD-induced suppression of IPSCs also were found. Our data suggest that a glutamate-like substance released from pyramidal cells could mediate CA1 DSI by reducing GABA release from interneurons via the activation of group I mGluRs.
Key words: IPSP; GABA; retrograde signal; voltage clamp; mGluR; synaptic inhibition
Copyright © 1998 Society for Neuroscience 0270-6474/98/18134870-13$05.00/0
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