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Article: Selective knockdown of gene expression of N-methyl-D-aspartate receptor one ameliorates parkinsonian motor symptom in 6-hydroxydopamine-lesioned rats

TitleSelective knockdown of gene expression of N-methyl-D-aspartate receptor one ameliorates parkinsonian motor symptom in 6-hydroxydopamine-lesioned rats
Authors
Issue Date2004
PublisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuint
Citation
Neurochemistry International, 2004, v. 45 n. 1, p. 11-22 How to Cite?
AbstractThe present study reported the efficacy of antisense oligonucleotides specific for N-methyl-D-aspartate receptor one (NR1) in reduction of motor symptom in a rat parkinsonian model, the unilateral 6-hydroxydopamine-lesioned rat. Significant reductions in apomorphine-induced contralateral rotation were only seen in the NR1 antisense-treated lesioned rats (after a single intraparenchymal dose of antisense to the lesioned neostriatum; 15nmol in 3μl of saline) at 1 or 2 days after the treatment. No motor effect was seen in the lesioned animals with control treatments (sham, treatment using NR1 sense oligonucleotides, randomized oligonucleotides or saline, respectively). In contrast, significant increases in expression of NR1 mRNA in the lesioned neostriatum were seen in rats with control treatments but not in rats with NR1 antisense treatment. Importantly, in the lesioned neostriatum that was treated with NR1 antisense, a significant reduction in NR1 protein expression was found and NR1 immunoreactivity was seen to reduce in perikarya of presumed striatal medium spiny neurons. The present data indicate that a single dose of NR1 antisense ameliorates motor symptom in the rat model. The efficacy of NR1 antisense is likely to be mediated by a selective knockdown in expression of NR1 mRNA and proteins in the presumed medium spiny neurons. © 2003 Elsevier Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/171733
ISSN
2015 Impact Factor: 3.385
2015 SCImago Journal Rankings: 1.345
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, SKen_US
dc.contributor.authorNg, TKYen_US
dc.contributor.authorLau, WKen_US
dc.contributor.authorYang, MSen_US
dc.contributor.authorWong, CKCen_US
dc.contributor.authorChan, YSen_US
dc.contributor.authorYung, KKLen_US
dc.date.accessioned2012-10-30T06:16:41Z-
dc.date.available2012-10-30T06:16:41Z-
dc.date.issued2004en_US
dc.identifier.citationNeurochemistry International, 2004, v. 45 n. 1, p. 11-22en_US
dc.identifier.issn0197-0186en_US
dc.identifier.urihttp://hdl.handle.net/10722/171733-
dc.description.abstractThe present study reported the efficacy of antisense oligonucleotides specific for N-methyl-D-aspartate receptor one (NR1) in reduction of motor symptom in a rat parkinsonian model, the unilateral 6-hydroxydopamine-lesioned rat. Significant reductions in apomorphine-induced contralateral rotation were only seen in the NR1 antisense-treated lesioned rats (after a single intraparenchymal dose of antisense to the lesioned neostriatum; 15nmol in 3μl of saline) at 1 or 2 days after the treatment. No motor effect was seen in the lesioned animals with control treatments (sham, treatment using NR1 sense oligonucleotides, randomized oligonucleotides or saline, respectively). In contrast, significant increases in expression of NR1 mRNA in the lesioned neostriatum were seen in rats with control treatments but not in rats with NR1 antisense treatment. Importantly, in the lesioned neostriatum that was treated with NR1 antisense, a significant reduction in NR1 protein expression was found and NR1 immunoreactivity was seen to reduce in perikarya of presumed striatal medium spiny neurons. The present data indicate that a single dose of NR1 antisense ameliorates motor symptom in the rat model. The efficacy of NR1 antisense is likely to be mediated by a selective knockdown in expression of NR1 mRNA and proteins in the presumed medium spiny neurons. © 2003 Elsevier Ltd. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Ltd. The Journal's web site is located at http://www.elsevier.com/locate/neuinten_US
dc.relation.ispartofNeurochemistry Internationalen_US
dc.rightsNeurochemistry International. Copyright © Elsevier Ltd.-
dc.subject.meshAnimalsen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulation - Drug Effects - Physiologyen_US
dc.subject.meshGene Silencing - Drug Effects - Physiologyen_US
dc.subject.meshMotor Activity - Drug Effects - Physiologyen_US
dc.subject.meshNeostriatum - Drug Effects - Metabolismen_US
dc.subject.meshOligonucleotides, Antisense - Pharmacologyen_US
dc.subject.meshOxidopamineen_US
dc.subject.meshParkinsonian Disorders - Chemically Induced - Genetics - Metabolismen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Sprague-Dawleyen_US
dc.subject.meshReceptors, N-Methyl-D-Aspartate - Antagonists & Inhibitors - Biosynthesisen_US
dc.titleSelective knockdown of gene expression of N-methyl-D-aspartate receptor one ameliorates parkinsonian motor symptom in 6-hydroxydopamine-lesioned ratsen_US
dc.typeArticleen_US
dc.identifier.emailChan, YS:yschan@hkucc.hku.hken_US
dc.identifier.emailLai, SK: estherlai@hkusua.hku.hk-
dc.identifier.emailTse, YC: tseyc@hkusua.hku.hk-
dc.identifier.emailLau, JWK: jaegerlau@yahoo.com.hk-
dc.identifier.authorityChan, YS=rp00318en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.neuint.2004.01.004en_US
dc.identifier.pmid15082217-
dc.identifier.scopuseid_2-s2.0-1842788129en_US
dc.identifier.hkuros92156-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1842788129&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume45en_US
dc.identifier.issue1en_US
dc.identifier.spage11en_US
dc.identifier.epage22en_US
dc.identifier.isiWOS:000221080600002-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridLai, SK=7402937165en_US
dc.identifier.scopusauthoridNg, TKY=36799700000en_US
dc.identifier.scopusauthoridLau, WK=7402933189en_US
dc.identifier.scopusauthoridYang, MS=7404925734en_US
dc.identifier.scopusauthoridWong, CKC=35276549400en_US
dc.identifier.scopusauthoridChan, YS=7403676627en_US
dc.identifier.scopusauthoridYung, KKL=13605496000en_US

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