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Article: Gene expression of glutamate receptors GluR1 and NR1 is differentially modulated in striatal neurons in rats after 6-hydroxydopamine lesion

TitleGene expression of glutamate receptors GluR1 and NR1 is differentially modulated in striatal neurons in rats after 6-hydroxydopamine lesion
Authors
KeywordsBasal ganglia
Etiology
Ionotropic glutamate receptors
Medium spiny neurons
Motor symptoms
Rat model of Parkinson's disease
Striatal interneurons
Issue Date2003
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuint
Citation
Neurochemistry International, 2003, v. 43 n. 7, p. 639-653 How to Cite?
AbstractIn the present study, we attempted to address the modulation of the gene expression of N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) glutamate receptors in the neostriatum of the 6-hydroxydopamine (6-OHDA)-lesioned rat, an animal model of Parkinson's disease. After 2 weeks of lesion, reverse transcriptase-polymerase chain reactions (RT-PCRs) revealed significant reduction in GluR1 mRNA expression but a significant enhancement of NR1 mRNA expression in the striatal tissues of the lesioned side. No modulation in the mRNA expression of GluR2, GluR3, GluR4 and NR2B were found. Immunofluorescence with digital imaging analysis also demonstrated a significant reduction in GluR1 immunoreactivity in the lesioned neostriatum. Interestingly, the reduction in GluR1 immunoreactivity was primarily observed in presumed striatal medium spiny neurons but not in parvalbumin-labeled striatal GABAergic interneurons. Immunoreactivity for GluR2, GluR2/3, GluR4, NR1 and NR2B was unchanged in neurons of the neostriatum of the lesioned side. The present results indicate that there is an opposite trend in modulation in the gene expressions of GluR1 and NR1 in the neostriatum of 6-OHDA-lesioned rats after dopamine denervation. Modulation of GluR1 mRNA and immunoreactivity is likely to be limited in the striatal projection neurons. These findings have implications for the use of NMDA and AMPA receptor antagonists in the treatment of Parkinson's disease. © 2003 Elsevier Science Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/81101
ISSN
2015 Impact Factor: 3.385
2015 SCImago Journal Rankings: 1.345
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, SKen_HK
dc.contributor.authorTse, YCen_HK
dc.contributor.authorYang, MSen_HK
dc.contributor.authorWong, CKCen_HK
dc.contributor.authorChan, YSen_HK
dc.contributor.authorYung, KKLen_HK
dc.date.accessioned2010-09-06T08:13:50Z-
dc.date.available2010-09-06T08:13:50Z-
dc.date.issued2003en_HK
dc.identifier.citationNeurochemistry International, 2003, v. 43 n. 7, p. 639-653en_HK
dc.identifier.issn0197-0186en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81101-
dc.description.abstractIn the present study, we attempted to address the modulation of the gene expression of N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) glutamate receptors in the neostriatum of the 6-hydroxydopamine (6-OHDA)-lesioned rat, an animal model of Parkinson's disease. After 2 weeks of lesion, reverse transcriptase-polymerase chain reactions (RT-PCRs) revealed significant reduction in GluR1 mRNA expression but a significant enhancement of NR1 mRNA expression in the striatal tissues of the lesioned side. No modulation in the mRNA expression of GluR2, GluR3, GluR4 and NR2B were found. Immunofluorescence with digital imaging analysis also demonstrated a significant reduction in GluR1 immunoreactivity in the lesioned neostriatum. Interestingly, the reduction in GluR1 immunoreactivity was primarily observed in presumed striatal medium spiny neurons but not in parvalbumin-labeled striatal GABAergic interneurons. Immunoreactivity for GluR2, GluR2/3, GluR4, NR1 and NR2B was unchanged in neurons of the neostriatum of the lesioned side. The present results indicate that there is an opposite trend in modulation in the gene expressions of GluR1 and NR1 in the neostriatum of 6-OHDA-lesioned rats after dopamine denervation. Modulation of GluR1 mRNA and immunoreactivity is likely to be limited in the striatal projection neurons. These findings have implications for the use of NMDA and AMPA receptor antagonists in the treatment of Parkinson's disease. © 2003 Elsevier Science Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuinten_HK
dc.relation.ispartofNeurochemistry Internationalen_HK
dc.rightsNeurochemistry International. Copyright © Elsevier Ltd.en_HK
dc.subjectBasal gangliaen_HK
dc.subjectEtiologyen_HK
dc.subjectIonotropic glutamate receptorsen_HK
dc.subjectMedium spiny neuronsen_HK
dc.subjectMotor symptomsen_HK
dc.subjectRat model of Parkinson's diseaseen_HK
dc.subjectStriatal interneuronsen_HK
dc.titleGene expression of glutamate receptors GluR1 and NR1 is differentially modulated in striatal neurons in rats after 6-hydroxydopamine lesionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0197-0186&volume=43&spage=639&epage=653&date=2003&atitle=Gene+expression+of+glutamate+receptors+GluR1+and+NR1+is+differentially+modulated+in+striatal+neurons+in+rats+after+6-hydroxydopamine+lesion.+++en_HK
dc.identifier.emailChan, YS: yschan@hkucc.hku.hken_HK
dc.identifier.authorityChan, YS=rp00318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0197-0186(03)00080-9en_HK
dc.identifier.pmid12892651-
dc.identifier.scopuseid_2-s2.0-0042208196en_HK
dc.identifier.hkuros82049en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0042208196&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume43en_HK
dc.identifier.issue7en_HK
dc.identifier.spage639en_HK
dc.identifier.epage653en_HK
dc.identifier.isiWOS:000184664100005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLai, SK=7402937165en_HK
dc.identifier.scopusauthoridTse, YC=7005116869en_HK
dc.identifier.scopusauthoridYang, MS=7404925734en_HK
dc.identifier.scopusauthoridWong, CKC=35276549400en_HK
dc.identifier.scopusauthoridChan, YS=7403676627en_HK
dc.identifier.scopusauthoridYung, KKL=13605496000en_HK

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