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The Journal of Neurophysiology Vol. 84 No. 5 November 2000, pp. 2284-2290
Copyright ©2000 by the American Physiological Society
Department of Neuroscience, University of Pennsylvania, Philadelphia, Pennsylvania 19104-6074
Dutar, Patrick,
Jeffrey J. Petrozzino,
Huan M. Vu,
Marc F. Schmidt, and
David J. Perkel.
Slow Synaptic Inhibition Mediated by Metabotropic Glutamate
Receptor Activation of GIRK Channels. J. Neurophysiol. 84: 2284-2290, 2000. Glutamate is the predominant
excitatory neurotransmitter in the vertebrate CNS. Ionotropic glutamate
receptors mediate fast excitatory actions whereas metabotropic
glutamate receptors (mGluRs) mediate a variety of slower effects. For
example, mGluRs can mediate presynaptic inhibition, postsynaptic
excitation, or, more rarely, postsynaptic inhibition. We previously
described an unusually slow form of postsynaptic inhibition in one
class of projection neuron in the song-control nucleus HVc of the
songbird forebrain. These neurons, which participate in a circuit that
is essential for vocal learning, exhibit an inhibitory postsynaptic
potential (IPSP) that lasts several seconds. Only a portion of this
slow IPSP is mediated by GABAB receptors. Since these cells
are strongly hyperpolarized by agonists of mGluRs, we used
intracellular recording from brain slices to investigate the mechanism
of this hyperpolarization and to determine whether mGluRs contribute to
the slow synaptic inhibition. We report that mGluRs hyperpolarize these
HVc neurons by activating G protein-coupled, inwardly-rectifying
potassium (GIRK) channels. MGluR antagonists blocked this response and
the slow synaptic inhibition. Thus, glutamate can combine with GABA to
mediate slow synaptic inhibition by activating GIRK channels in the CNS.
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