scholarly journals Excitatory Modulation in the Cochlear Nucleus through Group I Metabotropic Glutamate Receptor Activation

2011 ◽  
Vol 31 (20) ◽  
pp. 7450-7455 ◽  
Author(s):  
S. Chanda ◽  
M. A. Xu-Friedman
Keyword(s):  
Glutamate Receptor ◽  
Cochlear Nucleus ◽  
Metabotropic Glutamate Receptor ◽  
Receptor Activation ◽  
Metabotropic Glutamate ◽  
Group I

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

2009 ◽  
Vol 101 (4) ◽  
pp. 1761-1773 ◽  
Author(s):  
G. Govindaiah ◽  
Charles L. Cox
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Brightness Discrimination ◽  
Optic Tract ◽  
Gaba Release ◽  
Receptor Activation ◽  
Metabotropic Glutamate ◽  
Lateral Geniculate ◽  
Group I

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 GABAA 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 (2 R, 4 R)-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.

Metabotropic Glutamate Receptor Activation Modulates Sound Level Processing in the Cochlear Nucleus

1998 ◽  
Vol 80 (1) ◽  
pp. 209-217 ◽  
Author(s):  
Dan H. Sanes ◽  
JoAnn McGee ◽  
Edward J. Walsh
Keyword(s):  
Glutamate Receptors ◽  
Glutamate Receptor ◽  
Cochlear Nucleus ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Long Term Potentiation ◽  
Receptor Activation ◽  
Sound Level ◽  
Metabotropic Glutamate

Sanes, Dan H., JoAnn McGee, and Edward J. Walsh. Metabotropic glutamate receptor activation modulates sound level processing in the cochlear nucleus. J. Neurophysiol. 80: 209–217, 1998. The principal role of ionotropic glutamate receptors in the transmission and processing of information in the auditory pathway has been investigated extensively. In contrast, little is known about the functional contribution of the G-protein–coupled metabotropic glutamate receptors (mGluRs), although their anatomic location suggests that they exercise a significant influence on auditory processing. To investigate this issue, sound-evoked responses were obtained from single auditory neurons in the cochlear nuclear complex of anesthetized cats and gerbils, and metabotropic ligands were administered locally through microionophoretic pipettes. In general, microionophoresis of the mGluR agonists, (1 S,3 R)-1-aminocyclopentane-1,3-dicarboxylic acid or (2 S,1′ S,2′ S)-2-(carboxycyclopropyl)glycine, initially produced a gradual increase in spontaneous and sound-evoked discharge rates. However, activation and recovery times were significantly longer than those observed for ionotropic agonists, such as N-methyl-d-aspartate or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, consistent with the recruitment of a second-messenger system. The efficacy of mGluR agonists was diminished after administration of the mGluR antagonist, (+)-α-methyl-4-carboxyphenylglycine, consistent with a selective action at metabotropic recognition sites. In contrast, two distinct changes were observed after the mGluR agonist had been discontinued for several minutes. Approximately 50% of neurons exhibited a chronic depression of sound-evoked discharge rate reminiscent of long-term depression, a cellular property observed in other systems. Approximately 30% of neurons exhibited a long-lasting enhancement of the sound-evoked response similar to the cellular phenomenon of long-term potentiation. These findings suggest that mGluR activation has a profound influence on the gain of primary afferent driven activity in the caudal cochlear nucleus.

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