RGD Reference Report - Activation of neuropeptide Y Y1 receptors inhibits glutamate release through reduction of voltage-dependent Ca2+ entry in the rat cerebral cortex nerve terminals: suppression of this inhibitory effect by the protein kinase C-dependent facilitatory pathway. - Rat Genome Database

RGD Reference Report - Activation of neuropeptide Y Y1 receptors inhibits glutamate release through reduction of voltage-dependent Ca2+ entry in the rat cerebral cortex nerve terminals: suppression of this inhibitory effect by the protein kinase C-dependent facilitatory pathway. - Rat Genome Database

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General

Activation of neuropeptide Y Y1 receptors inhibits glutamate release through reduction of voltage-dependent Ca2+ entry in the rat cerebral cortex nerve terminals: suppression of this inhibitory effect by the protein kinase C-dependent facilitatory pathway.
Authors:	Wang, S-J
Citation:	Wang SJ, Neuroscience. 2005;134(3):987-1000. doi: 10.1016/j.neuroscience.2005.04.053.
RGD ID:	155230755
Pubmed:	PMID:16026936 (View Abstract at PubMed)
DOI:	DOI:10.1016/j.neuroscience.2005.04.053 (Journal Full-text)
Neuropeptide Y (NPY) is known to regulate the presynaptic glutamate release and neuronal responses to excitatory neurotransmission. The aim of this study was to investigate the effect of NPY on the release of endogenous glutamate from rat cerebrocortical nerve terminals (synaptosomes). NPY inhibited the Ca2+-dependent glutamate release evoked by 4-aminopyridine, and this inhibitory effect was mediated via NPY Y1 receptors, because it was mimicked by the specific NPY Y1 receptor agonist [Leu31 Pro34] NPY and blocked by the NPY Y1 receptor antagonist GR 231118. The inhibitory action of NPY was not due to it decreasing synaptosomal excitability or directly interfering with the release process at some point subsequent to Ca2+ influx, because NPY did not alter the 4-aminopyridine-evoked depolarization of the synaptosomal plasma membrane potential or ionomycin and hypertonic solution-induced glutamate release. Examination of the effect of NPY on the cytosolic [Ca2+] revealed that the inhibition of glutamate release could be attributed to a reduction in voltage-dependent Ca2+ influx. Consistent with this, the NPY-mediated inhibition of glutamate release was completely abolished in synaptosomes pretreated with N- and P/Q-type Ca2+ channel blocker, omega-conotoxin MVIIC. Moreover, NPY-mediated inhibition of 4-aminopyridine-evoked glutamate release was insensitive to KT 5720 and Ro32-0432 but was suppressed when protein kinase C was stimulated with phorbol ester. Together, these results suggest that NPY acting predominantly on NPY Y1 receptors inhibits glutamate release from rat cerebrocortical synaptosomes, likely by a mechanism involving direct coupling of receptors to N- and P/Q-type Ca2+ channels, and this coupling is subject to regulation by protein kinase C-dependent pathway. This implies that selective ligand for NPY receptors may be of value for treatment of conditions characterized by excessive glutamate release in the cerebral cortex.

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Biological Process

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Term	Qualifier	Evidence	With	Reference	Notes	Source	Original Reference(s)
regulation of presynaptic cytosolic calcium ion concentration	involved_in	EXP		155230755; 155230755	PMID:16026936	SynGO
regulation of presynaptic cytosolic calcium ion concentration	involved_in	IDA		155230755; 155230755	PMID:16026936	SynGO
regulation of synaptic vesicle exocytosis	involved_in	EXP		155230755; 155230755	PMID:16026936	SynGO
regulation of synaptic vesicle exocytosis	involved_in	IDA		155230755; 155230755	PMID:16026936	SynGO

Objects Annotated

Genes (Rattus norvegicus)

Npy (neuropeptide Y)

Npy1r (neuropeptide Y receptor Y1)

Additional Information