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Opiate alkaloids antagonize postsynaptic glycine and GABA responses: Correlation with convulsant action

dc.contributor.authorWerz, Mary Annen_US
dc.contributor.authorMacDonald, Robert L.en_US
dc.date.accessioned2006-04-07T17:53:39Z
dc.date.available2006-04-07T17:53:39Z
dc.date.issued1982-03-18en_US
dc.identifier.citationWerz, Mary Ann, MacDonald, Robert L. (1982/03/18)."Opiate alkaloids antagonize postsynaptic glycine and GABA responses: Correlation with convulsant action." Brain Research 236(1): 107-119. <http://hdl.handle.net/2027.42/24031>en_US
dc.identifier.urihttp://www.sciencedirect.com/science/article/B6SYR-4836007-1DJ/2/c40285947fab3bf58ab4db494780c6dben_US
dc.identifier.urihttps://hdl.handle.net/2027.42/24031
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=7066678&dopt=citationen_US
dc.description.abstractOpiate alkaloid and opioid peptide actions on spontaneous neuronal activity and postsynaptic amino acid responsiveness were assessed using intracellular recording techniques applied to murine spinal cord neurons in primary dissociated cell culture. Application of opiates was by superfusion and amino acids by iontophoresis. Glycine and GABA but not glutamate responses were antagonized by the opiate alkaloids. Since opiate effects on glycine and GABA responses were not naloxone-reversible, only weakly stereospecific, and not produced by the opioid peptide [-Ala2]-Met-enkephalinamide, it is unlikely that these effects were mediated by opiate receptors. Opiate depression of glycine inhibition was correlated with the induction of paroxysmal depolarizations in cultured spinal cord neurons, suggesting that antagonism of inhibitory amino acid transmission may underlie the convulsant actions of high concentrations of the opiate alkaloids.en_US
dc.format.extent752158 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherElsevieren_US
dc.titleOpiate alkaloids antagonize postsynaptic glycine and GABA responses: Correlation with convulsant actionen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelPublic Healthen_US
dc.subject.hlbsecondlevelNeurosciencesen_US
dc.subject.hlbsecondlevelMolecular, Cellular and Developmental Biologyen_US
dc.subject.hlbtoplevelScienceen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumNeurosciences Program, University of Michigan Medical Center, Neuroscience Laboratory Building, 1103 East Huron, Ann Arbor, MI 48109, U.S.A.; (R.L.M.) Department of Neurology, University of Michigan Medical Center, Neuroscience Laboratory Building, 1103 East Huron, Ann Arbor, MI 48109, U.S.A.en_US
dc.contributor.affiliationumNeurosciences Program, University of Michigan Medical Center, Neuroscience Laboratory Building, 1103 East Huron, Ann Arbor, MI 48109, U.S.A.; (R.L.M.) Department of Neurology, University of Michigan Medical Center, Neuroscience Laboratory Building, 1103 East Huron, Ann Arbor, MI 48109, U.S.A.en_US
dc.identifier.pmid7066678en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/24031/1/0000280.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1016/0006-8993(82)90038-5en_US
dc.identifier.sourceBrain Researchen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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