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NAAG peptidase inhibitor increases dialysate NAAG and reduces glutamate, aspartate and GABA levels in the dorsal hippocampus following fluid percussion injury in the rat

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dc.contributor.author Zhong, Chunlong
dc.contributor.author Zhao, Xueren
dc.contributor.author Van, Ken C.
dc.contributor.author Bzdega, Tomasz
dc.contributor.author Smyth, Aoife
dc.contributor.author Zhou, Zia
dc.contributor.author Kozikowski, Alan P.
dc.contributor.author Jiang, Jiyao
dc.contributor.author O'Connor, William T.
dc.contributor.author Berman, Robert F.
dc.contributor.author Neale, Joseph H.
dc.contributor.author Lyeth, Bruce G.
dc.date.accessioned 2015-09-23T14:10:15Z
dc.date.available 2015-09-23T14:10:15Z
dc.date.issued 2006
dc.identifier.citation Zhong, C; Zhao, XR; Van, KC; Bzdega, T; Smyth, A; Zhou, J; Kozikowski, AP; Jiang, JY; O'Connor, WT; Berman, RF; Neale, JH; Lyeth, BG (2006) ''NAAG peptidase inhibitor increases dialysate NAAG and reduces glutamate, aspartate and GABA levels in the dorsal hippocampus following fluid percussion injury in the rat'. JOURNAL OF NEUROCHEMISTRY, 97 (4):1015-1025. en_US
dc.identifier.uri http://hdl.handle.net/10344/4654
dc.description peer-reviewed en_US
dc.description.abstract Traumatic brain injury (TBI) produces a rapid and excessive elevation in extracellular glutamate that induces excitotoxic brain cell death. The peptide neurotransmitter N-acetylaspartylglutamate (NAAG) is reported to suppress neurotransmitter release through selective activation of presynaptic Group II metabotropic glutamate receptors. Therefore, strategies to elevate levels of NAAG following brain injury could reduce excessive glutamate release associated with TBI. We hypothesized that the NAAG peptidase IIlhih itor. ZJ-43 would elevate extracellul~lr NAAG levels and reduce ext",cellular levels of amino acid neurotransmitters following Tl3l by a Group II metabotropic glutamate receptor (mGluR)-mcdiated mechanism. Dialysate levels ofNAAG, glutamate, aspartate and GABA from the dorsal hippocampus were elevated after TBI as measured by ill vivo microdialysis. Dialysate levels ofNAAG were higher and remained elevated in the ZJ-43 treated group (50 mg/kg, i.p.) compared to control. ZJ-43 treatment also reduced the rise of dialysate glutamate, aspartate, and GAB A levels. Co-administration of the Group II mGluR antagonist, L Y34 1495 (I mg/kg, i.p.) partially blocked the effects of ZJ-43 on dialysate glutamate and GABA suggesting that NAAG effects are mediated through mGluR activation. The results are consistent with the hypothesis that inhibition ofNAAG peptidase may reduce excitotoxic events associated with TBI. en_US
dc.language.iso eng en_US
dc.publisher Wiley en_US
dc.relation.ispartofseries Journal of Neurochemistry;97 (4), pp. 1015-1025
dc.relation.uri http://dx.doi.org/10.1111/j.1471-4159.2006.03786.x
dc.rights This is the author's version of the following article: NAAG peptidase inhibitor increases dialysate NAAG and reduces glutamate, aspartate and GABA levels in the dorsal hippocampus following fluid percussion injury in the ratThe definitive version is available at http://dx.doi.org/10.1111/j.1471-4159.2006.03786.x en_US
dc.subject traumatic brain injury en_US
dc.subject glutamate en_US
dc.subject N-acetylaspartylglutamate (NAAG) en_US
dc.subject microdialysis en_US
dc.subject metabotropic glutamate receptor en_US
dc.title NAAG peptidase inhibitor increases dialysate NAAG and reduces glutamate, aspartate and GABA levels in the dorsal hippocampus following fluid percussion injury in the rat en_US
dc.type info:eu-repo/semantics/article en_US
dc.type.supercollection all_ul_research en_US
dc.type.supercollection ul_published_reviewed en_US
dc.date.updated 2015-09-23T13:35:42Z
dc.description.version ACCEPTED
dc.contributor.sponsor National Neuroscience Network (Ireland) en_US
dc.contributor.sponsor EI en_US
dc.contributor.sponsor SFI en_US
dc.rights.accessrights info:eu-repo/semantics/openAccess en_US
dc.internal.rssid 1120746
dc.internal.copyrightchecked Yes
dc.identifier.journaltitle JOURNAL OF NEUROCHEMISTRY
dc.description.status peer-reviewed


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