| Electrophysiological effects of neuropeptide S on rat ventromedial hypothalamic neurons in vitro. | |
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MedLine Citation:
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PMID: 19925841 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The newly identified neuropeptide S (NPS) is a ligand for a previously orphan G protein-coupled GPR 154 receptor, now named the NPS receptor (NPSR). Previous studies have shown that NPS induces hyperlocomotion, increases arousal and suppresses anxiety-like behaviors via NPSR. Although NPS also inhibits food intake, nothing is known about the neuronal mechanisms underlying this action. Anatomical studies show that NPSRs are expressed abundantly in the dorsomedial part of the ventromedial hypothalamic nucleus (VMH), a satiety center for food intake. Hence, we examined the electrophysiological effects of NPS on rat VMH neurons in vitro. NPS predominantly depolarized the VMH neurons, and the effects were postsynaptic and dose-dependent. Membrane resistance was significantly decreased during the depolarization, suggesting an opening of some ionic channels. The NPS-induced depolarization was significantly attenuated in Ca(2+)-free, NiCl(2)-containing and mibefradil-containing TTX ACSFs, but it did not disappear. The NPS-induced depolarization was also attenuated in low-Na(+) TTX ACSF, and completely abolished in Ca(2+)-free/low-Na(+) TTX ACSF. Pretreatment with 30 microM KB-R7943, an inhibitor of forward-mode Na(+)/Ca(2+) exchanger, did not have any significant effect on the NPS-induced depolarization in Ca(2+)-free TTX ACSF. These results suggest that NPS depolarizes VMH neurons via activations of R- and T-type Ca(2+) channels and nonselective cation channels, and that VMH neurons might be involved in the cellular process through which NPS participates in the regulation of food intake and energy homeostasis. |
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Authors:
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Keitaro Yoshida; Juhyon Kim; Kazuki Nakajima; Yutaka Oomura; Matthew J Wayner; Kazuo Sasaki |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2009-11-17 |
Journal Detail:
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Title: Peptides Volume: 31 ISSN: 1873-5169 ISO Abbreviation: Peptides Publication Date: 2010 Apr |
Date Detail:
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Created Date: 2010-03-12 Completed Date: 2010-07-01 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8008690 Medline TA: Peptides Country: United States |
Other Details:
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Languages: eng Pagination: 712-9 Citation Subset: IM |
Copyright Information:
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Copyright (c) 2009 Elsevier Inc. All rights reserved. |
Affiliation:
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Division of Bio-Information Engineering, Faculty of Engineering, University of Toyama, 3190 Gofuku, Toyama 930-8555, Japan. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Calcium / metabolism Calcium Channel Blockers / pharmacology Dose-Response Relationship, Drug Electrophysiological Phenomena / drug effects* Male Mibefradil / pharmacology Neurons / cytology, drug effects, physiology Neuropeptides / pharmacology* Nickel / pharmacology Patch-Clamp Techniques Rats Rats, Wistar Sodium / metabolism Sodium Channel Blockers / pharmacology Tetrodotoxin / pharmacology Ventromedial Hypothalamic Nucleus / cytology*, drug effects*, physiology |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channel Blockers; 0/Neuropeptides; 0/Sodium Channel Blockers; 116644-53-2/Mibefradil; 4368-28-9/Tetrodotoxin; 7440-02-0/Nickel; 7440-23-5/Sodium; 7440-70-2/Calcium; 7718-54-9/nickel chloride |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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