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Roles of transient receptor potential vanilloid subtype 1 and cannabinoid type 1 receptors in the brain: neuroprotection versus neurotoxicity.

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dc.contributor.authorKim, SR-
dc.contributor.authorChung, YC-
dc.contributor.authorChung, ES-
dc.contributor.authorPark, KW-
dc.contributor.authorWon, SY-
dc.contributor.authorBok, E-
dc.contributor.authorPark, ES-
dc.contributor.authorJin, BK-
dc.date.accessioned2011-03-17T05:21:00Z-
dc.date.available2011-03-17T05:21:00Z-
dc.date.issued2007-
dc.identifier.issn0893-7648-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/1791-
dc.description.abstractTransient receptor potential vanilloid subtype 1 (TRPV1), also known as vanilloid receptor 1 (VR1), is a nonselective cation channel that is activated by a variety of ligands, such as exogenous capsaicin (CAP) or endogenous anandamide (AEA), as well as products of lipoxygenases. Cannabinoid type 1 (CB1) receptor belongs to the G protein-coupled receptor superfamily and is activated by cannabinoids such as AEA and exogenous Delta-9-tetrahydrocannabinol (THC). TRPV1 and CB1 receptors are widely expressed in the brain and play many significant roles in various brain regions; however, the issue of whether TRPV1 or CB1 receptors mediate neuroprotection or neurotoxicity remains controversial. Furthermore, functional crosstalk between these two receptors has been recently reported. It is therefore timely to review current knowledge regarding the functions of these two receptors and to consider new directions of investigation on their roles in the brain.-
dc.language.isoen-
dc.subject.MESHAnimals-
dc.subject.MESHArachidonic Acids-
dc.subject.MESHBrain-
dc.subject.MESHCapsaicin-
dc.subject.MESHEndocannabinoids-
dc.subject.MESHNeuroprotective Agents-
dc.subject.MESHPolyunsaturated Alkamides-
dc.subject.MESHReceptor, Cannabinoid, CB1-
dc.subject.MESHSensory System Agents-
dc.subject.MESHTRPV Cation Channels-
dc.titleRoles of transient receptor potential vanilloid subtype 1 and cannabinoid type 1 receptors in the brain: neuroprotection versus neurotoxicity.-
dc.typeArticle-
dc.identifier.pmid17917113-
dc.contributor.affiliatedAuthor정, 은숙-
dc.contributor.affiliatedAuthor진, 병관-
dc.type.localJournal Papers-
dc.citation.titleMolecular neurobiology-
dc.citation.volume35-
dc.citation.number3-
dc.citation.date2007-
dc.citation.startPage245-
dc.citation.endPage254-
dc.identifier.bibliographicCitationMolecular neurobiology, 35(3). : 245-254, 2007-
dc.identifier.eissn1559-1182-
dc.relation.journalidJ008937648-
Appears in Collections:
Journal Papers > Research Organization > BK21
Journal Papers > Research Organization > Institute for Medical Sciences
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