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Article: Neurokinin receptor 3 peptide exacerbates 6-hydroxydopamine-induced dopaminergic degeneration in rats through JNK pathway

TitleNeurokinin receptor 3 peptide exacerbates 6-hydroxydopamine-induced dopaminergic degeneration in rats through JNK pathway
Authors
Issue Date2012
PublisherBlackwell Publishing Ltd. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1471-4159
Citation
Journal of Neurochemistry, 2012, v. 123 n. 3, p. 417-427 How to Cite?
AbstractNeurokinin 3 (NK3) receptor is predominantly expressed in striatum and substantia nigra (SN). Evidences have indicated the roles of NK3 receptor in the pathogenesis of Parkinson's disease. By administrating NK3 receptor agonist senktide into 6-hydroxydopamine (6-OHDA)-lesioned rats, exacerbation of dopaminergic degeneration was found in striatum and substantia nigra pars compacta. From apomorphine rotation test, significant increase of contralateral rotation number was detected in 6-OHDA-lesioned rats with senktide injection. Furthermore, tyrosine hydroxylase expression in striatum and substantia nigra pars compacta were examined by immunohistochemistry and Western blotting. Further reduction of tyrosine hydroxylase immunoreactivities was found in 6-OHDA-lesioned rats that received senktide treatment. Also, phosphorylation of N-methyl-D-aspartate receptor 1 subunit was investigated in SN region and significant up-regulation was revealed in senktide-treated 6-OHDA-lesioned rats. Finally, phosphorylation of mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) and c-Jun were examined in nigral region. Up-regulation of phosphorylated JNK molecules was shown in SN region after senktide injection. In line with this evidence, phosphorylation of c-Jun at Ser 63 and Ser 73 was also up-regulated by senktide treatment, thus presenting new aspects that NK3 peptide could exacerbate 6-OHDA toxicity in in vivo models and the possible mechanism may be contributed by the modulation of N-methyl-D-aspartate receptor 1 subunit and JNK pathway activities.
Persistent Identifierhttp://hdl.handle.net/10722/184663
ISSN
2023 Impact Factor: 4.2
2023 SCImago Journal Rankings: 1.476
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChu, JMT-
dc.contributor.authorChan, YS-
dc.contributor.authorChen, LW-
dc.contributor.authorYung, KKL-
dc.date.accessioned2013-07-15T10:02:31Z-
dc.date.available2013-07-15T10:02:31Z-
dc.date.issued2012-
dc.identifier.citationJournal of Neurochemistry, 2012, v. 123 n. 3, p. 417-427-
dc.identifier.issn0022-3042-
dc.identifier.urihttp://hdl.handle.net/10722/184663-
dc.description.abstractNeurokinin 3 (NK3) receptor is predominantly expressed in striatum and substantia nigra (SN). Evidences have indicated the roles of NK3 receptor in the pathogenesis of Parkinson's disease. By administrating NK3 receptor agonist senktide into 6-hydroxydopamine (6-OHDA)-lesioned rats, exacerbation of dopaminergic degeneration was found in striatum and substantia nigra pars compacta. From apomorphine rotation test, significant increase of contralateral rotation number was detected in 6-OHDA-lesioned rats with senktide injection. Furthermore, tyrosine hydroxylase expression in striatum and substantia nigra pars compacta were examined by immunohistochemistry and Western blotting. Further reduction of tyrosine hydroxylase immunoreactivities was found in 6-OHDA-lesioned rats that received senktide treatment. Also, phosphorylation of N-methyl-D-aspartate receptor 1 subunit was investigated in SN region and significant up-regulation was revealed in senktide-treated 6-OHDA-lesioned rats. Finally, phosphorylation of mitogen-activated protein kinase c-Jun N-terminal kinase (JNK) and c-Jun were examined in nigral region. Up-regulation of phosphorylated JNK molecules was shown in SN region after senktide injection. In line with this evidence, phosphorylation of c-Jun at Ser 63 and Ser 73 was also up-regulated by senktide treatment, thus presenting new aspects that NK3 peptide could exacerbate 6-OHDA toxicity in in vivo models and the possible mechanism may be contributed by the modulation of N-methyl-D-aspartate receptor 1 subunit and JNK pathway activities.-
dc.languageeng-
dc.publisherBlackwell Publishing Ltd. The Journal's web site is located at http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1471-4159-
dc.relation.ispartofJournal of Neurochemistry-
dc.rightsThe definitive version is available at www.blackwell-synergy.com-
dc.subject.meshCorpus Striatum - metabolism - pathology-
dc.subject.meshDopaminergic Neurons - metabolism - pathology-
dc.subject.meshMAP Kinase Signaling System - physiology-
dc.subject.meshNerve Degeneration - metabolism - pathology-
dc.subject.meshReceptors, Neurokinin-3 - agonists - antagonists and inhibitors - physiology-
dc.titleNeurokinin receptor 3 peptide exacerbates 6-hydroxydopamine-induced dopaminergic degeneration in rats through JNK pathway-
dc.typeArticle-
dc.identifier.emailChan, YS: yschan@hku.hk-
dc.identifier.authorityChan, YS=rp00318-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1471-4159.2012.07858.x-
dc.identifier.pmid22762252-
dc.identifier.scopuseid_2-s2.0-84867336094-
dc.identifier.hkuros216059-
dc.identifier.volume123-
dc.identifier.issue3-
dc.identifier.spage417-
dc.identifier.epage427-
dc.identifier.isiWOS:000309743600010-
dc.publisher.placeUnited Kingdom-

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