Group I metabotropic glutamate receptor activation induces TRPC6-dependent calcium influx and RhoA activation in cultured human kidney podocytes

2019 ◽  
Vol 511 (2) ◽  
pp. 374-380 ◽  
Author(s):  
Qin Wang ◽  
Derun Wang ◽  
Shigeru Shibata ◽  
Tianrong Ji ◽  
Lei Zhang ◽  
...  
Keyword(s):  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Calcium Influx ◽  
Human Kidney ◽  
Receptor Activation ◽  
Metabotropic Glutamate ◽  
Rhoa Activation ◽  
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.

Group I Metabotropic Glutamate Receptor Activation Produces a Direct Excitation of Identified Septohippocampal Cholinergic Neurons

2004 ◽  
Vol 92 (2) ◽  
pp. 1216-1225 ◽  
Author(s):  
Min Wu ◽  
Tibor Hajszan ◽  
Changqing Xu ◽  
Csaba Leranth ◽  
Meenakshi Alreja
Keyword(s):  
Glutamate Receptor ◽  
Neurodegenerative Disorders ◽  
Metabotropic Glutamate Receptors ◽  
Metabotropic Glutamate Receptor ◽  
Cholinergic Neurons ◽  
Receptor Activation ◽  
Receptor Subtypes ◽  
Metabotropic Glutamate ◽  
Group I ◽  
Double Immunolabeling

Septohippocampal cholinergic neurons innervate the hippocampus and provide it with almost its entire acetylcholine. Axon collaterals of these neurons also release acetylcholine within the septum and thereby maintain the firing activity of septohippocampal GABAergic neurons. A loss of septohippocampal cholinergic neurons occurs in various neurodegenerative disorders associated with cognitive dysfunctions. group I metabotropic glutamate receptors have been implicated in septohippocampal-dependent learning and memory tasks. In the present study, we examined the physiological and pharmacological effects of a potent and selective group I metabotropic glutamate receptor (mGluR) agonist S-3,5-dihydroxyphenylglycine (DHPG) on rat septohippocampal cholinergic neurons that were identified in brain slices using a selective fluorescent marker. In whole cell recordings, DHPG produced a reversible, reproducible and a direct postsynaptic and concentration-dependent excitation in 100% of septohippocampal cholinergic neurons tested with an EC50 of 2.1 μM. Pharmacologically, the effects of DHPG were partially/completely reduced by the mGluR1 antagonists, 7-hydrox-iminocyclopropan[b]chromen-1a-carboxylic acid ethyl ester and (+)-2-methyl-4-carboxyphenylglycine. Addition of the mGluR5 antagonist, 2-methyl-6-(phenylethnyl)pyridine hydrochloride, reduced the remaining response to DHPG, suggesting involvement of both receptor subtypes in a subpopulation of septohippocampal cholinergic neurons. In double-immunolabeling studies, 74% of septohippocampal cholinergic neurons co-localized mGluR1α-immunoreactivity and 35% co-localized mGluR5-immunoreactivity. Double-immunolabeling studies at the light and electron-microscopic levels showed that vesicular glutamate transporter 2 terminals make asymmetric synaptic contacts with septohippocampal cholinergic neurons. These findings may be of significance in treatment of cognitive deficits associated with neurodegenerative disorders as a group I mGluR-mediated activation of septohippocampal cholinergic neurons would enhance the release of acetylcholine both in the hippocampus and in the septum.

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