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Article: Neuropeptide changes following excitotoxic lesion of the insular cortex in rats

TitleNeuropeptide changes following excitotoxic lesion of the insular cortex in rats
Authors
Issue Date1995
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, 1995, v. 362 n. 4, p. 535-550 How to Cite?
AbstractFollowing middle cerebral artery occlusion in Wistar rats, the immunoreactivity of neuropeptide Y increased ipsilaterally in the insular cortex and basolateral nucleus of the amygdala. In addition, the immunoreactivity of leucine-enkephalin, dynorphin, and neurotensin increased in the ipsilateral central nucleus of the amygdala. The amygdalar neurochemical changes are likely the result of damage to the insular cortex, although other cortical areas were also affected by the ischemia. To investigate whether damage to the insular cortex is essential in eliciting these changes, a localized lesion of the right or left insular cortex was produced by microinjection of D,L-homocysteic acid. Control animals received injections of vehicle into the right or left insular cortex or D,L- homocysteic acid into the right primary somatosensory cortex. Neurochemical changes were examined immunohistochemically with the peroxidase- antiperoxidase reaction 5 days after the injection. The immunoreactivity of neuropeptide Y increased locally after excitotoxic damage to the insular cortex or primary somatosensory cortex. The amygdalar neurochemical changes, including neuropeptide Y increase in the basolateral nucleus and leucine- enkephalin, dynorphin, and neurotensin increase in the central nucleus, were seen only when the ipsilateral insular cortex was lesioned. These neurochemical changes were similar to those seen 5 days after middle cerebral artery occlusion. Our findings indicate that damage to the insular cortex is essential in eliciting the neurochemical changes in the ipsilateral amygdala. In addition, the change in neuropeptide Y in the cortex appears to be a local reaction occurring irrespective of location of the lesion and glutamate receptor activation may be involved.
Persistent Identifierhttp://hdl.handle.net/10722/162074
ISSN
2015 Impact Factor: 3.331
2015 SCImago Journal Rankings: 2.345
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCheung, RTFen_US
dc.contributor.authorCechetto, DFen_US
dc.date.accessioned2012-09-05T05:17:05Z-
dc.date.available2012-09-05T05:17:05Z-
dc.date.issued1995en_US
dc.identifier.citationJournal Of Comparative Neurology, 1995, v. 362 n. 4, p. 535-550en_US
dc.identifier.issn0021-9967en_US
dc.identifier.urihttp://hdl.handle.net/10722/162074-
dc.description.abstractFollowing middle cerebral artery occlusion in Wistar rats, the immunoreactivity of neuropeptide Y increased ipsilaterally in the insular cortex and basolateral nucleus of the amygdala. In addition, the immunoreactivity of leucine-enkephalin, dynorphin, and neurotensin increased in the ipsilateral central nucleus of the amygdala. The amygdalar neurochemical changes are likely the result of damage to the insular cortex, although other cortical areas were also affected by the ischemia. To investigate whether damage to the insular cortex is essential in eliciting these changes, a localized lesion of the right or left insular cortex was produced by microinjection of D,L-homocysteic acid. Control animals received injections of vehicle into the right or left insular cortex or D,L- homocysteic acid into the right primary somatosensory cortex. Neurochemical changes were examined immunohistochemically with the peroxidase- antiperoxidase reaction 5 days after the injection. The immunoreactivity of neuropeptide Y increased locally after excitotoxic damage to the insular cortex or primary somatosensory cortex. The amygdalar neurochemical changes, including neuropeptide Y increase in the basolateral nucleus and leucine- enkephalin, dynorphin, and neurotensin increase in the central nucleus, were seen only when the ipsilateral insular cortex was lesioned. These neurochemical changes were similar to those seen 5 days after middle cerebral artery occlusion. Our findings indicate that damage to the insular cortex is essential in eliciting the neurochemical changes in the ipsilateral amygdala. In addition, the change in neuropeptide Y in the cortex appears to be a local reaction occurring irrespective of location of the lesion and glutamate receptor activation may be involved.en_US
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/31248en_US
dc.relation.ispartofJournal of Comparative Neurologyen_US
dc.subject.meshAmygdala - Chemistry - Drug Effects - Metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCerebral Cortex - Chemistry - Drug Effects - Metabolismen_US
dc.subject.meshDynorphins - Analysis - Metabolismen_US
dc.subject.meshEnkephalin, Leucine - Analysis - Metabolismen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMaleen_US
dc.subject.meshNeuropeptide Y - Analysis - Metabolismen_US
dc.subject.meshNeuropeptides - Analysis - Metabolismen_US
dc.subject.meshNeurotensin - Analysis - Metabolismen_US
dc.subject.meshNeurotoxins - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRats, Wistar - Physiologyen_US
dc.titleNeuropeptide changes following excitotoxic lesion of the insular cortex 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.doi10.1002/cne.903620408en_US
dc.identifier.pmid8636466-
dc.identifier.scopuseid_2-s2.0-0028892014en_US
dc.identifier.volume362en_US
dc.identifier.issue4en_US
dc.identifier.spage535en_US
dc.identifier.epage550en_US
dc.identifier.isiWOS:A1995TH22200007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCheung, RTF=7202397498en_US
dc.identifier.scopusauthoridCechetto, DF=7006226109en_US

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