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Article: Neurochemical changes following occlusion of the middle cerebral artery in rats

TitleNeurochemical changes following occlusion of the middle cerebral artery in rats
Authors
Issue Date1995
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscience
Citation
Neuroscience, 1995, v. 68 n. 4, p. 1037-1050 How to Cite?
AbstractWe have developed a stroke model involving middle cerebral artery occlusion in the rat which elicits changes in cardiac and autonomic variables that are similar to those observed clinically. It is likely that these neurogenic autonomic responses are mediated by changes in neurotransmitter systems subsequent to the stroke. This possibility was investigated by examining changes in immunohistochemical staining for tyrosine hydroxylase, neuropeptide Y, leu-enkephalin, neurotensin and dynorphin following middle cerebral artery occlusion in the rat. Computerized image analysis was used to provide semi-quantitative measurements of the changes. The ischemic region was centered primarily in the insular cortex. The results indicate that there are significant increases in immunostaining for tyrosine hydroxylase and neuropeptide Y in the insular cortex within the peri-infarct region. Neuropeptide Y staining was also significantly increased in the basolateral nucleus of the amygdala, ipsilateral to the middle cerebral artery occlusion, which did not appear to be included in the infarct. Leu-enkephalin, neurotensin and dynorphin staining was significantly elevated in the central nucleus of the amygdala ipsilateral to the occlusion of the middle cerebral artery. These neurochemical changes are discussed as possible mechanisms mediating the cardiac and autonomic consequences of stroke or as part of a process to provide neuro-protection following focal cerebral ischemia.
Persistent Identifierhttp://hdl.handle.net/10722/162102
ISSN
2015 Impact Factor: 3.231
2015 SCImago Journal Rankings: 1.768
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorAllen, GVen_US
dc.contributor.authorCheung, RTFen_US
dc.contributor.authorCechetto, DFen_US
dc.date.accessioned2012-09-05T05:17:21Z-
dc.date.available2012-09-05T05:17:21Z-
dc.date.issued1995en_US
dc.identifier.citationNeuroscience, 1995, v. 68 n. 4, p. 1037-1050en_US
dc.identifier.issn0306-4522en_US
dc.identifier.urihttp://hdl.handle.net/10722/162102-
dc.description.abstractWe have developed a stroke model involving middle cerebral artery occlusion in the rat which elicits changes in cardiac and autonomic variables that are similar to those observed clinically. It is likely that these neurogenic autonomic responses are mediated by changes in neurotransmitter systems subsequent to the stroke. This possibility was investigated by examining changes in immunohistochemical staining for tyrosine hydroxylase, neuropeptide Y, leu-enkephalin, neurotensin and dynorphin following middle cerebral artery occlusion in the rat. Computerized image analysis was used to provide semi-quantitative measurements of the changes. The ischemic region was centered primarily in the insular cortex. The results indicate that there are significant increases in immunostaining for tyrosine hydroxylase and neuropeptide Y in the insular cortex within the peri-infarct region. Neuropeptide Y staining was also significantly increased in the basolateral nucleus of the amygdala, ipsilateral to the middle cerebral artery occlusion, which did not appear to be included in the infarct. Leu-enkephalin, neurotensin and dynorphin staining was significantly elevated in the central nucleus of the amygdala ipsilateral to the occlusion of the middle cerebral artery. These neurochemical changes are discussed as possible mechanisms mediating the cardiac and autonomic consequences of stroke or as part of a process to provide neuro-protection following focal cerebral ischemia.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/neuroscienceen_US
dc.relation.ispartofNeuroscienceen_US
dc.subject.meshAmygdala - Metabolism - Pathologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBrain Chemistry - Physiologyen_US
dc.subject.meshBrain Ischemia - Metabolism - Pathologyen_US
dc.subject.meshBrain Stem - Metabolism - Pathologyen_US
dc.subject.meshCerebral Arteries - Physiologyen_US
dc.subject.meshCerebral Cortex - Pathologyen_US
dc.subject.meshCerebral Infarction - Pathologyen_US
dc.subject.meshDynorphins - Pharmacologyen_US
dc.subject.meshEnkephalin, Leucine - Pharmacologyen_US
dc.subject.meshImage Processing, Computer-Assisteden_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMaleen_US
dc.subject.meshPrefrontal Cortex - Pathologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistaren_US
dc.subject.meshTyrosine 3-Monooxygenase - Metabolismen_US
dc.titleNeurochemical changes following occlusion of the middle cerebral artery in ratsen_US
dc.typeArticleen_US
dc.identifier.emailCheung, RTF:rtcheung@hku.hken_US
dc.identifier.authorityCheung, RTF=rp00434en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/0306-4522(95)00198-Ren_US
dc.identifier.pmid8544980en_US
dc.identifier.scopuseid_2-s2.0-0029123305en_US
dc.identifier.volume68en_US
dc.identifier.issue4en_US
dc.identifier.spage1037en_US
dc.identifier.epage1050en_US
dc.identifier.isiWOS:A1995RW40000008-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridAllen, GV=7402366127en_US
dc.identifier.scopusauthoridCheung, RTF=7202397498en_US
dc.identifier.scopusauthoridCechetto, DF=7006226109en_US

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