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Article: Colchicine affects cortical and amygdalar neurochemical changes differentially after middle cerebral artery occlusion in rats

TitleColchicine affects cortical and amygdalar neurochemical changes differentially after middle cerebral artery occlusion in rats
Authors
Issue Date1997
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, 1997, v. 387 n. 1, p. 27-41 How to Cite?
AbstractRecently, we have shown increases in the immunoreactivity for neuropeptide Y and tyrosine hydroxylase in the insular cortex surrounding the focal infarction after middle cerebral artery occlusion. In addition, the immunoreactivity for neuropeptide Y, leucine-enkephalin, dynorphin, and neurotensin increased ipsilaterally in the amygdala. Increases in immunoreactivity were observed in nerve terminals and fibers; changes in the neuropeptides were maximal 3 days after stroke. Local excitotoxic injury of the insular cortex also elicited similar neuropeptide changes unilaterally in the same regions. In this study, immunohistochemistry was used following intracerebroventricular injection of colchicine and stroke to determine whether blockade of axonal transport would prevent these neurochemical changes. These experiments would also locate the putative cellular origins of the neurochemicals involved. Control rats received either colchicine injection or middle cerebral artery occlusion alone. Injection of colchicine enhanced the periinfarct increase in neuropeptide Y but did not alter the increase in tyrosine hydroxylase. The neuropeptide Y increase was observed in local cortical neurons. Colchicine prevented the increases in immunoreactivity for the neuropeptides in the amygdala on the side of stroke, although there were small perikarya that showed immunoreactivity for these neuropeptides within the amygdala on both sides. We conclude that local cortical neurons are responsible for the increase in neuropeptide Y in the periinfarct region, that the cortical increase in tyrosine hydroxylase is not dependent on fast axonal transport, and that axonal transport of signals from the insular cortex to the amygdala is critical in mediating the amygdalar neuropeptide changes seen after stroke.
Persistent Identifierhttp://hdl.handle.net/10722/76791
ISSN
2015 Impact Factor: 3.331
2015 SCImago Journal Rankings: 2.345
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheung, RTFen_HK
dc.contributor.authorCechetto, DFen_HK
dc.date.accessioned2010-09-06T07:24:57Z-
dc.date.available2010-09-06T07:24:57Z-
dc.date.issued1997en_HK
dc.identifier.citationJournal Of Comparative Neurology, 1997, v. 387 n. 1, p. 27-41en_HK
dc.identifier.issn0021-9967en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76791-
dc.description.abstractRecently, we have shown increases in the immunoreactivity for neuropeptide Y and tyrosine hydroxylase in the insular cortex surrounding the focal infarction after middle cerebral artery occlusion. In addition, the immunoreactivity for neuropeptide Y, leucine-enkephalin, dynorphin, and neurotensin increased ipsilaterally in the amygdala. Increases in immunoreactivity were observed in nerve terminals and fibers; changes in the neuropeptides were maximal 3 days after stroke. Local excitotoxic injury of the insular cortex also elicited similar neuropeptide changes unilaterally in the same regions. In this study, immunohistochemistry was used following intracerebroventricular injection of colchicine and stroke to determine whether blockade of axonal transport would prevent these neurochemical changes. These experiments would also locate the putative cellular origins of the neurochemicals involved. Control rats received either colchicine injection or middle cerebral artery occlusion alone. Injection of colchicine enhanced the periinfarct increase in neuropeptide Y but did not alter the increase in tyrosine hydroxylase. The neuropeptide Y increase was observed in local cortical neurons. Colchicine prevented the increases in immunoreactivity for the neuropeptides in the amygdala on the side of stroke, although there were small perikarya that showed immunoreactivity for these neuropeptides within the amygdala on both sides. We conclude that local cortical neurons are responsible for the increase in neuropeptide Y in the periinfarct region, that the cortical increase in tyrosine hydroxylase is not dependent on fast axonal transport, and that axonal transport of signals from the insular cortex to the amygdala is critical in mediating the amygdalar neuropeptide changes seen after stroke.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31248en_HK
dc.relation.ispartofJournal of Comparative Neurologyen_HK
dc.subject.meshAmygdala - drug effects - metabolismen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshArterial Occlusive Diseases - metabolismen_HK
dc.subject.meshAxonal Transport - drug effectsen_HK
dc.subject.meshCerebral Arteries - metabolismen_HK
dc.subject.meshCerebral Cortex - drug effects - metabolismen_HK
dc.subject.meshCerebral Infarction - pathologyen_HK
dc.subject.meshColchicine - pharmacologyen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshInjections, Intraventricularen_HK
dc.subject.meshMaleen_HK
dc.subject.meshRatsen_HK
dc.subject.meshRats, Wistaren_HK
dc.titleColchicine affects cortical and amygdalar neurochemical changes differentially after middle cerebral artery occlusion in ratsen_HK
dc.typeArticleen_HK
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_HK
dc.identifier.authorityCheung, RTF=rp00434en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/(SICI)1096-9861(19971013)387:1<27::AID-CNE3>3.0.CO;2-Pen_HK
dc.identifier.pmid9331169-
dc.identifier.scopuseid_2-s2.0-0030883978en_HK
dc.identifier.hkuros52673en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0030883978&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume387en_HK
dc.identifier.issue1en_HK
dc.identifier.spage27en_HK
dc.identifier.epage41en_HK
dc.identifier.isiWOS:A1997XZ20400003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheung, RTF=7202397498en_HK
dc.identifier.scopusauthoridCechetto, DF=7006226109en_HK

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