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Article: Downregulation of glial glutamate transporters after dopamine denervation in the striatum of 6-hydroxydopamine-lesioned rats

TitleDownregulation of glial glutamate transporters after dopamine denervation in the striatum of 6-hydroxydopamine-lesioned rats
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31248
Citation
Journal Of Comparative Neurology, 2008, v. 511 n. 4, p. 421-437 How to Cite?
AbstractOveractivity of glutamatergic neurotransmission in the basal ganglia is known to be closely related to the onset and pathogenesis of Parkinson's disease. Glutamate homeostasis around glutamatergic synapses is tightly regulated by two groups of glutamate transporters: glial glutamate transporters GLT1 (EAAT2) and GLAST (EAAT1), and neuronal glutamate transporter EAAC1. In order to investigate the changes of glutamate transporters after the onset of Parkinson's disease, unilateral 6-hydroxydopamine-lesioned rat, an animal model of Parkinson's disease, was employed. By immunofluorescence and Western blot analyses, GLT1 and GLAST proteins were significantly reduced in the striatum with lesion. No change in GLT1 and GLAST protein was found in the substantia nigra. The reduction of GLT1 protein in the striatum was more prominent than that of GLAST protein (∼40% vs. 20%). In addition, EAAC1 protein was found to be increased in the substantia nigra pars reticulata of the lesioned rats but not in the striatum. The present results indicate that reductions of GLT1 and GLAST may impair glutamate homeostasis around glutamatergic synapses in the striatum and contribute to over-spills of glutamate in the system. An increase in the EAAC1 level in the substantia nigra pars reticulata may increase GABA synthesis and enhance GABAergic neurotransmission. These results indicate that there are differential and distinct modulations of glutamate transporters after dopamine denervation in the 6-hydroxydopamine-lesioned rat. © 2008 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/171776
ISSN
2015 Impact Factor: 3.331
2015 SCImago Journal Rankings: 2.345
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.accessioned2012-10-30T06:16:59Z-
dc.date.available2012-10-30T06:16:59Z-
dc.date.issued2008en_US
dc.identifier.citationJournal Of Comparative Neurology, 2008, v. 511 n. 4, p. 421-437en_US
dc.identifier.issn0021-9967en_US
dc.identifier.urihttp://hdl.handle.net/10722/171776-
dc.description.abstractOveractivity of glutamatergic neurotransmission in the basal ganglia is known to be closely related to the onset and pathogenesis of Parkinson's disease. Glutamate homeostasis around glutamatergic synapses is tightly regulated by two groups of glutamate transporters: glial glutamate transporters GLT1 (EAAT2) and GLAST (EAAT1), and neuronal glutamate transporter EAAC1. In order to investigate the changes of glutamate transporters after the onset of Parkinson's disease, unilateral 6-hydroxydopamine-lesioned rat, an animal model of Parkinson's disease, was employed. By immunofluorescence and Western blot analyses, GLT1 and GLAST proteins were significantly reduced in the striatum with lesion. No change in GLT1 and GLAST protein was found in the substantia nigra. The reduction of GLT1 protein in the striatum was more prominent than that of GLAST protein (∼40% vs. 20%). In addition, EAAC1 protein was found to be increased in the substantia nigra pars reticulata of the lesioned rats but not in the striatum. The present results indicate that reductions of GLT1 and GLAST may impair glutamate homeostasis around glutamatergic synapses in the striatum and contribute to over-spills of glutamate in the system. An increase in the EAAC1 level in the substantia nigra pars reticulata may increase GABA synthesis and enhance GABAergic neurotransmission. These results indicate that there are differential and distinct modulations of glutamate transporters after dopamine denervation in the 6-hydroxydopamine-lesioned rat. © 2008 Wiley-Liss, Inc.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31248en_US
dc.relation.ispartofJournal of Comparative Neurologyen_US
dc.subject.meshAdrenergic Agents - Toxicityen_US
dc.subject.meshAmino Acid Transport System X-Ag - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCorpus Striatum - Drug Effects - Metabolismen_US
dc.subject.meshDenervationen_US
dc.subject.meshDopamine - Metabolismen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshFemaleen_US
dc.subject.meshFluorescent Antibody Techniqueen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshNeuroglia - Metabolismen_US
dc.subject.meshOxidopamine - Toxicityen_US
dc.subject.meshParkinsonian Disorders - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.titleDownregulation of glial glutamate transporters after dopamine denervation in the 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.doi10.1002/cne.21852en_US
dc.identifier.pmid18831527en_US
dc.identifier.scopuseid_2-s2.0-58149277182en_US
dc.identifier.hkuros164088-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-58149277182&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume511en_US
dc.identifier.issue4en_US
dc.identifier.spage421en_US
dc.identifier.epage437en_US
dc.identifier.isiWOS:000260842000001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridChung, EKY=16315234600en_US
dc.identifier.scopusauthoridChen, LW=25937158100en_US
dc.identifier.scopusauthoridChan, YS=7403676627en_US
dc.identifier.scopusauthoridYung, KKL=13605496000en_US

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