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Article: Up-regulation in expression of vesicular glutamate transporter 3 in substantia nigra but not in striatum of 6-hydroxydopamine-lesioned rats

TitleUp-regulation in expression of vesicular glutamate transporter 3 in substantia nigra but not in striatum of 6-hydroxydopamine-lesioned rats
Authors
Issue Date2007
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Neurosignals, 2007, v. 15 n. 5, p. 238-248 How to Cite?
AbstractOveractivity of the glutamatergic system is suggested to be closely related to the onset and pathogenesis of Parkinson's disease. Vesicular glutamate transporters (VGLUT1, T2 and T3) are a group of glutamate transporters in neurons that are responsible for transporting glutamate into synaptic vesicles and they are key elements for homeostasis of glutamate neurotransmission. The present study was aimed to investigate the expression of VGLUT1, T2 and T3 proteins after the onset of Parkinson's disease. A rat model of Parkinson's disease, the 6-hydroxydopamine-lesioned rat, was employed. Immunocytochemistry revealed that VGLUT1, T2 and T3 immunoreactivity was not modulated in the striatum of the lesioned rat. Western blotting analyses also showed that there was no change in the expression of T1, T2 and T3 proteins in the striatum. In contrast, no VGLUT1 protein was detected in the substantia nigra. After the lesion, levels of VGLUT2 immunoreactivity and protein were not modulated. Significant increase of VGLUT3 immunoreactivity was observed in the perikarya of GABAergic substantia nigra pars reticulata neurons (+14.7%) although VGLUT3 protein was not modulated in the nigral tissues. VGLUT3 in GABAergic neurons is suggested to play a role in GABA synthesis. The present results may therefore implicate that VGLUT1 and T2 are not modulated in the striatum and the substantia nigra of the 6-hydroxydopamine-lesioned rat and only VGLUT3 plays a role in pathogenesis of Parkinson's disease. Copyright © 2007 S. Karger AG.
Persistent Identifierhttp://hdl.handle.net/10722/171760
ISSN
2015 Impact Factor: 1.593
2015 SCImago Journal Rankings: 0.763
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChung, EKYen_US
dc.contributor.authorChen, LWen_US
dc.contributor.authorChan, YSen_US
dc.contributor.authorYung, KKLen_US
dc.date.accessioned2012-10-30T06:16:50Z-
dc.date.available2012-10-30T06:16:50Z-
dc.date.issued2007en_US
dc.identifier.citationNeurosignals, 2007, v. 15 n. 5, p. 238-248en_US
dc.identifier.issn1424-862Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/171760-
dc.description.abstractOveractivity of the glutamatergic system is suggested to be closely related to the onset and pathogenesis of Parkinson's disease. Vesicular glutamate transporters (VGLUT1, T2 and T3) are a group of glutamate transporters in neurons that are responsible for transporting glutamate into synaptic vesicles and they are key elements for homeostasis of glutamate neurotransmission. The present study was aimed to investigate the expression of VGLUT1, T2 and T3 proteins after the onset of Parkinson's disease. A rat model of Parkinson's disease, the 6-hydroxydopamine-lesioned rat, was employed. Immunocytochemistry revealed that VGLUT1, T2 and T3 immunoreactivity was not modulated in the striatum of the lesioned rat. Western blotting analyses also showed that there was no change in the expression of T1, T2 and T3 proteins in the striatum. In contrast, no VGLUT1 protein was detected in the substantia nigra. After the lesion, levels of VGLUT2 immunoreactivity and protein were not modulated. Significant increase of VGLUT3 immunoreactivity was observed in the perikarya of GABAergic substantia nigra pars reticulata neurons (+14.7%) although VGLUT3 protein was not modulated in the nigral tissues. VGLUT3 in GABAergic neurons is suggested to play a role in GABA synthesis. The present results may therefore implicate that VGLUT1 and T2 are not modulated in the striatum and the substantia nigra of the 6-hydroxydopamine-lesioned rat and only VGLUT3 plays a role in pathogenesis of Parkinson's disease. Copyright © 2007 S. Karger AG.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_US
dc.relation.ispartofNeuroSignalsen_US
dc.rightsNeuroSignals. Copyright © S Karger AG.-
dc.subject.meshAnalysis Of Varianceen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBehavior, Animal - Drug Effectsen_US
dc.subject.meshCorpus Striatum - Drug Effects - Metabolismen_US
dc.subject.meshDihydroxyphenylalanine - Analogs & Derivatives - Toxicityen_US
dc.subject.meshDisease Models, Animalen_US
dc.subject.meshFemaleen_US
dc.subject.meshParkinson Disease - Etiology - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshRotarod Performance Test - Methodsen_US
dc.subject.meshSubstantia Nigra - Drug Effects - Metabolismen_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.subject.meshVesicular Glutamate Transport Proteins - Metabolismen_US
dc.titleUp-regulation in expression of vesicular glutamate transporter 3 in substantia nigra but not in striatum of 6-hydroxydopamine-lesioned ratsen_US
dc.typeArticleen_US
dc.identifier.emailChan, YS:yschan@hkucc.hku.hken_US
dc.identifier.authorityChan, YS=rp00318en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1159/000101704en_US
dc.identifier.pmid17435391-
dc.identifier.scopuseid_2-s2.0-34547956841en_US
dc.identifier.hkuros149576-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34547956841&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume15en_US
dc.identifier.issue5en_US
dc.identifier.spage238en_US
dc.identifier.epage248en_US
dc.identifier.isiWOS:000248237500003-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridChung, EKY=16315234600en_US
dc.identifier.scopusauthoridChen, LW=7409444941en_US
dc.identifier.scopusauthoridChan, YS=7403676627en_US
dc.identifier.scopusauthoridYung, KKL=13605496000en_US
dc.identifier.citeulike6428977-

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