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dc.contributor.authorJohnston, Michael V.en_US
dc.date.accessioned2007-04-06T18:49:19Z
dc.date.available2007-04-06T18:49:19Z
dc.date.issued1983-05en_US
dc.identifier.citationJohnston, Michael V. (1983)."Neurotransmitter alterations in a model of perinatal hypoxic-ischemic brain injury." Annals of Neurology 13(5): 511-518. <http://hdl.handle.net/2027.42/50300>en_US
dc.identifier.issn0364-5134en_US
dc.identifier.issn1531-8249en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50300
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=6135388&dopt=citationen_US
dc.description.abstractVulnerability of neurotransmitter-specific neurons to hypoxia-ischemia was examined in the immature rat corpus striatum. Carotid artery ligation plus 2 hours of 8% oxygen atmosphere at 1 week of age produced ipsilateral striatal injury and reduced hemisphere mass 2 and 6 weeks later. Striatal injury was always more severe than damage to overlying cortex. Over half the animals had status marmoratus, a neuropathological change seen in the basal ganglia and thalamus after hypoxic-ischemic injury in full-term human infants. Two weeks after the insult, markers for choinergic, dopaminergic, and Γ-aminobutyric acid–containing neurons were all reduced, but the reduction in cholinergic markers was greater than that for the other two transmitters. Muscarinic cholinergic receptors were relatively preserved, but their distribution was disrupted. In adult animals specific activity of cholinergic neuronal markers was normal, suggesting that the balance of neurotransmitters was restored after the early insult.en_US
dc.format.extent931316 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
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dc.publisherWiley Subscription Services, Inc., A Wiley Companyen_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherNeuroscience, Neurology, and Psychiatryen_US
dc.titleNeurotransmitter alterations in a model of perinatal hypoxic-ischemic brain injuryen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPsychiatryen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartments of Pediatrics and Neurology, University of Michigan Medical School and Center for Human Growth and Development, 1013 Neuroscience Bldg, 1103 E Huron, Ann Arbor, MI 48109 ; Departments of Pediatrics and Neurology, University of Michigan Medical School and Center for Human Growth and Development, 1013 Neuroscience Bldg, 1103 E Huron, Ann Arbor, MI 48109en_US
dc.identifier.pmid6135388en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50300/1/410130507_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/ana.410130507en_US
dc.identifier.sourceAnnals of Neurologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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