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This Article Full Text Full Text (PDF) All Versions of this Article: 101/4/1761    most recent 91107.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Govindaiah, G. Articles by Cox, C. L. Search for Related Content PubMed PubMed Citation Articles by Govindaiah, G. Articles by Cox, C. L.

Distinct Roles of Metabotropic Glutamate Receptor Activation on Inhibitory Signaling in the Ventral Lateral Geniculate Nucleus

Department of Pharmacology, College of Medicine and Department of Molecular and Integrative Physiology, Beckman Institute for Advanced Science and Technology, University of Illinois, Urbana, Illinois

Submitted 3 October 2008; accepted in final form 22 January 2009

The ventral lateral geniculate nucleus (vLGN) has been implicated in numerous functions including circadian rhythms, brightness discrimination, pupillary light reflex, and other visuomotor functions. The contribution of inhibitory mechanisms in the regulation of vLGN neuron excitability remains unexplored. We examined the actions of metabotropic glutamate receptor (mGluR) activation on the intrinsic excitability and inhibitory synaptic transmission in different lamina of vLGN. Activation of mGluRs exerts distinct pre- and postsynaptic actions in vLGN neurons. In the lateral magnocellular subdivision of vLGN (vLGNl), the general mGluR agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) enhanced the frequency of GABA_A receptor-mediated spontaneous inhibitory postsynaptic currents (sIPSC) that persisted in the presence of sodium channel blocker tetrodotoxin (TTX) in a subpopulation of neurons (TTX insensitive). This increase is attributed to the increased output of dendritic GABA release from vLGN interneurons. In contrast, in the medial subdivision of vLGN (vLGNm), the mGluR agonist-mediated increase in sIPSC frequency was completely blocked by TTX. The selective Group I mGluR agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) increased sIPSC frequency, whereas the selective Group II mGluR agonist (2R, 4R)-4-aminopyrrolidine-2,4-dicarboxylate (APDC) significantly decreased sIPSC frequency in vLGNl neurons. Optic tract stimulation also produced an mGluR-dependent increase in sIPSC frequency in vLGNl neurons. In contrast, we were unable to synaptically evoke alterations in sIPSC activity in vLGNm neurons. In addition to these presynaptic actions, DHPG depolarized both vLGNl and vLGNm neurons. In vLGN interneurons, mGluR activation produced opposing actions: APDC hyperpolarized the membrane potential, whereas DHPG produced a membrane depolarization. The present findings demonstrate diverse actions of mGluRs on vLGN neurons localized within different vLGN lamina. Considering these different lamina are coupled with distinct functional roles, thus these diverse actions may be involved in distinctive forms of visual and visuomotor information processing.