Abnormal cholecystokinin mRNA levels in entorhinal cortex of schizophrenics

dc.contributor.authorBachus, Susan E.
dc.contributor.authorHyde, Thomas M.
dc.contributor.authorHerman, Mary M.
dc.contributor.authorEgan, Michael F.
dc.contributor.authorKleinman, Joel E.
dc.date.accessioned2020-04-08T18:27:08Z
dc.date.available2020-04-08T18:27:08Z
dc.date.issued1998-01-05
dc.description.abstractLimbic cortical regions, including anterior cingulate cortex (ACC), prefrontal cortex (PFC) and entorhinal cortex (ERC), have been implicated in the neuropathology of schizophrenia. Glutamate projection neurons connect these limbic cortical regions to each other, as well as to the terminal fields of the striatal/accumbens dopamine neurons. Subsets of these glutamate projection neurons, and of the GABA interneurons in cortex, contain the neuropeptide cholecystokinin (CCK). In an effort to study the limbic cortical glutamate projection neurons and GABA interneurons in schizophrenia, we have measured CCK mRNA with in situ hybridization histochemistry in postmortem samples of dorsolateral (DL)PFC, ACC and ERC of seven schizophrenics, nine nonpsychotic suicides and seven normal controls. CCK mRNA is decreased in ERC (especially layers iii–vi) and subiculum in schizophrenics relative to controls. Cellular analysis indicates that there is a decrease in density of CCK mRNA in labelled neurons. In so far as ERC CCK mRNA is not reduced in rats treated chronically with haloperidol, this decrease in schizophrenics does not appear to be related to neuroleptic treatment. In contrast, in DLPFC, where schizophrenics do not differ from normals, the suicide victims have elevated CCK mRNA (especially in layers v and vi), and increased cellular density of CCK mRNA, relative to both normals and schizophrenics. These results lend further support for the involvement of ERC and hippocampus in schizophrenia, suggesting that neurons that utilize CCK may be particularly important. Similarly, an increase in CCK mRNA levels in the PFC of suicides adds to a growing body of evidence implicating this structure in this pathological state. In so far as CCK is co-localized with GABA or glutamate in cortical neurons, both of these neuronal populations need to be studied further in schizophrenia and suicide.en_US
dc.description.urihttps://www.sciencedirect.com/science/article/abs/pii/S0022395696000416?via%3Dihuben_US
dc.format.extent24 pagesen_US
dc.genrejournal articlesen_US
dc.identifierdoi:10.13016/m20m7u-akgv
dc.identifier.citationBachus, Susan E.; Hyde, Thomas M.; Herman, Mary M.; Egan, Michael F.; Kleinman, Joel E.; Abnormal cholecystokinin mRNA levels in entorhinal cortex of schizophrenics; Journal of Psychiatric Research 31(2), Pages 233-256 (1998); https://www.sciencedirect.com/science/article/abs/pii/S0022395696000416?via%3Dihub;en_US
dc.identifier.urihttps://doi.org/10.1016/S0022-3956(96)00041-6
dc.identifier.urihttp://hdl.handle.net/11603/17884
dc.language.isoen_USen_US
dc.publisherElsevieren_US
dc.relation.isAvailableAtThe University of Maryland, Baltimore County (UMBC)
dc.relation.ispartofUMBC Psychology Department Collection
dc.rightsThis item is likely protected under Title 17 of the U.S. Copyright Law. Unless on a Creative Commons license, for uses protected by Copyright Law, contact the copyright holder or the author.
dc.rightsPublic Domain Mark 1.0*
dc.rightsThis work was written as part of one of the author's official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law.
dc.rights.urihttp://creativecommons.org/publicdomain/mark/1.0/*
dc.titleAbnormal cholecystokinin mRNA levels in entorhinal cortex of schizophrenicsen_US
dc.typeTexten_US

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