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Article: Ablation of gene expression of N-methyl-D-aspartate receptor one by antisense oligonucleotides in striatal neurons in culture

TitleAblation of gene expression of N-methyl-D-aspartate receptor one by antisense oligonucleotides in striatal neurons in culture
Authors
KeywordsBasal ganglia
Gene therapy
Glutamate excitotoxicity
Immunofluorescence
Ionotropic glutamate receptors
Neostriatum
Neuronal cell death
Neuroprotection
Patch clamp
Reverse transcriptase-polymerase chain reaction
Issue Date2006
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Neurosignals, 2006, v. 14 n. 6, p. 303-316 How to Cite?
AbstractIn the present study, a twenty-mer antisense oligonucleotide specific for N-methyl-D-aspartate receptor one (ANR1) was applied to striatal neurons in primary cell culture. The ANR1 was found to be specific and nontoxic. Significant reductions in expression of NR1 mRNA and proteins were resulted after a single dose of ANR1 transcripts. Interestingly, there were reductions in total NR1 proteins but two phosphorylated forms of NR1 proteins at serine 896 and 897 residues were not reduced. There was also no change in the pattern of distribution of NR1 immunoreactivity in the striatal neurons. In addition, significant reductions of NMDA-mediated peak inward current were found after application of a higher concentration of ANR1 (20-100 μM) by patch clamp recordings. The present results indicate that ANR1 is a useful agent in reducing NMDA receptor functions. The present data thus provide detailed cellular and molecular mechanisms to explain our previous findings of amelioration of motor symptoms in a rat model of Parkinson's disease. More importantly, application of ANR1 was also found to display neuroprotective effects of striatal neurons against NMDA-induced excitotoxic cell death. The findings have implications in development of new approach in prevention of cell death in neurodegenerative diseases and new treatments for these diseases. Copyright © 2005 S. Karger AG.
Persistent Identifierhttp://hdl.handle.net/10722/81229
ISSN
2015 Impact Factor: 1.593
2015 SCImago Journal Rankings: 0.763
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLui, PWen_HK
dc.contributor.authorYeung, CWen_HK
dc.contributor.authorYung, WHen_HK
dc.contributor.authorShi, Yen_HK
dc.contributor.authorChen, LWen_HK
dc.contributor.authorChan, YSen_HK
dc.contributor.authorYung, KKLen_HK
dc.date.accessioned2010-09-06T08:15:17Z-
dc.date.available2010-09-06T08:15:17Z-
dc.date.issued2006en_HK
dc.identifier.citationNeurosignals, 2006, v. 14 n. 6, p. 303-316en_HK
dc.identifier.issn1424-862Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/81229-
dc.description.abstractIn the present study, a twenty-mer antisense oligonucleotide specific for N-methyl-D-aspartate receptor one (ANR1) was applied to striatal neurons in primary cell culture. The ANR1 was found to be specific and nontoxic. Significant reductions in expression of NR1 mRNA and proteins were resulted after a single dose of ANR1 transcripts. Interestingly, there were reductions in total NR1 proteins but two phosphorylated forms of NR1 proteins at serine 896 and 897 residues were not reduced. There was also no change in the pattern of distribution of NR1 immunoreactivity in the striatal neurons. In addition, significant reductions of NMDA-mediated peak inward current were found after application of a higher concentration of ANR1 (20-100 μM) by patch clamp recordings. The present results indicate that ANR1 is a useful agent in reducing NMDA receptor functions. The present data thus provide detailed cellular and molecular mechanisms to explain our previous findings of amelioration of motor symptoms in a rat model of Parkinson's disease. More importantly, application of ANR1 was also found to display neuroprotective effects of striatal neurons against NMDA-induced excitotoxic cell death. The findings have implications in development of new approach in prevention of cell death in neurodegenerative diseases and new treatments for these diseases. Copyright © 2005 S. Karger AG.en_HK
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_HK
dc.relation.ispartofNeuroSignalsen_HK
dc.rightsNeuroSignals. Copyright © S Karger AG.en_HK
dc.subjectBasal gangliaen_HK
dc.subjectGene therapyen_HK
dc.subjectGlutamate excitotoxicityen_HK
dc.subjectImmunofluorescenceen_HK
dc.subjectIonotropic glutamate receptorsen_HK
dc.subjectNeostriatumen_HK
dc.subjectNeuronal cell deathen_HK
dc.subjectNeuroprotectionen_HK
dc.subjectPatch clampen_HK
dc.subjectReverse transcriptase-polymerase chain reactionen_HK
dc.titleAblation of gene expression of N-methyl-D-aspartate receptor one by antisense oligonucleotides in striatal neurons in cultureen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1424-862X&volume=14&issue=6&spage=303&epage=316&date=2006&atitle=Ablation+of+gene+expression+of+N-methyl-D-aspartate+receptor+one+by+antisense+oligonucleotides+in+striatal+neurons+in+cultureen_HK
dc.identifier.emailChan, YS: yschan@hkucc.hku.hken_HK
dc.identifier.authorityChan, YS=rp00318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1159/000093045en_HK
dc.identifier.pmid16772733-
dc.identifier.scopuseid_2-s2.0-33745032015en_HK
dc.identifier.hkuros121707en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745032015&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume14en_HK
dc.identifier.issue6en_HK
dc.identifier.spage303en_HK
dc.identifier.epage316en_HK
dc.identifier.isiWOS:000238565400004-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridLui, PW=36916492100en_HK
dc.identifier.scopusauthoridYeung, CW=36848789000en_HK
dc.identifier.scopusauthoridYung, WH=7103137893en_HK
dc.identifier.scopusauthoridShi, Y=7404963860en_HK
dc.identifier.scopusauthoridChen, LW=7409444941en_HK
dc.identifier.scopusauthoridChan, YS=7403676627en_HK
dc.identifier.scopusauthoridYung, KKL=13605496000en_HK

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