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The Journal of Neuroscience, August 1, 1999, 19(15):6694-6699
Glutamate Inhibits Thalamic Reticular Neurons
Charles L. Cox and S. Murray Sherman Department of Neurobiology, State University of New York, Stony Brook, New York 11794-5230
Activation of metabotropic glutamate receptors (mGluRs) can result in long-lasting modulation of neuronal excitability. Multiple mGluR subtypes are localized within the rat thalamic reticular nucleus (TRN), and we have examined the effects of activating these different receptor subtypes on the excitability of these neurons using an in vitro slice preparation. Typical of most mGluR-sensitive preparations, the general mGluR agonist, (±)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (ACPD) produced a robust, long-lasting excitatory response. Surprisingly, ACPD produced a membrane hyperpolarization in some neurons. Using selective mGluR agonists, we found that activation of group II mGluRs produces the hyperpolarization, whereas the depolarization is mediated by group I mGluRs. While the polarity of the postsynaptic response (hyperpolarization vs depolarization) was dependent on the mGluR subtype activated, both actions appear to result from modification of a linear K+ conductance. The inhibitory action of Glutamate, via group II mGluRs, provides an avenue for a disinhibitory effect that could have interesting consequences upon a well-investigated, model neuronal circuit, turning its assumed functional role upside down.
Key words: thalamus; metabotropic glutamate receptors; thalamic reticular nucleus; inhibition; thalamocortical
Copyright © 1999 Society for Neuroscience 0270-6474/99/19156694-06$05.00/0
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