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dc.contributor.authorDure, Leon S. IVen_US
dc.contributor.authorYoung, Anne B.en_US
dc.contributor.authorPenney, John B.en_US
dc.date.accessioned2007-04-06T18:54:23Z
dc.date.available2007-04-06T18:54:23Z
dc.date.issued1991-12en_US
dc.identifier.citationDure, Leon S.; Young, Anne B.; Penney, John B. (1991)."Excitatory amino acid binding sites in the caudate nucleus and frontal cortex of huntington's disease." Annals of Neurology 30(6): 785-793. <http://hdl.handle.net/2027.42/50348>en_US
dc.identifier.issn0364-5134en_US
dc.identifier.issn1531-8249en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/50348
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=1665055&dopt=citationen_US
dc.description.abstractHuntington's disease is a dominantly inherited, progressive neurodegenerative disorder causing marked pathology in the basal ganglia. The pathophysiology of the selective neuronal death in as yet unknown, but evidence suggests that the neurotoxicity may result from endogenous substances acting at excitatory amino acid receptors. Previous data have shown a selective decrease in binding to one class of glutamate receptors, the N -methyl-D-aspartate (NMDA) receptor in the putamen of Huntington's disease. The present study was undertaken to determine the relative density of binding to all of the currently defined subpopulations of excitatory amino acid receptors in the caudate nuclei and frontal cortex of patients with Huntington's disease and of control subjects, using quantitative in vitro autoradiography. NMDA, MK-801, glycine, kainate, and Α-amino-3-hydroxy-5-methylisoxazole propionic acid (AMPA) receptor binding were all decreased to a similar extent (50–60°). Binding to the metabotropic quisqualate receptor and to the non-NMDA, nonkainate, nonquisqualate (NNKQ) site was decreased nonsignificantly by 31° and 26°, respectively. Autoradiograms of NMDA, MK-801, AMPA, kainate, metabotropic, and NNKQ receptors in caudates revealed an inhomogeneous pattern of binding that is different from the binding pattern seen in control caudates. Binding to all receptor subtypes was the same in the frontal cortex from Huntington's disease patients and control subjects. The data suggest that no single excitatory amino acid receptor is selectively decreased in the caudate of Huntington's disease.en_US
dc.format.extent874066 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.titleExcitatory amino acid binding sites in the caudate nucleus and frontal cortex of huntington's diseaseen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPsychiatryen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan, Ann Arbor, MI ; Massachusetts General Hospital, Neurology Research, Wellman 415, Boston, MA 02114en_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan, Ann Arbor, MIen_US
dc.contributor.affiliationumDepartment of Neurology, University of Michigan, Ann Arbor, MIen_US
dc.identifier.pmid1665055en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/50348/1/410300607_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/ana.410300607en_US
dc.identifier.sourceAnnals of Neurologyen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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