Source:http://linkedlifedata.com/resource/pubmed/id/12082566
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
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| pubmed:dateCreated |
2002-6-25
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| pubmed:abstractText |
Recent imaging and postmortem studies suggest that impaired connectivity is involved in the pathophysiology of schizophrenia and major affective disorders. We investigated the presynaptic proteins complexin (Cx) I and Cx II in postmortem prefrontal cortex in schizophrenia (n = 13; six suicide, seven nonsuicide), major depression (n= 11, all suicide) and controls (n = 11) with an enzyme-linked immunoadsorbent assay (ELISA). Overall analysis indicated a significant difference between groups (F = 3.93, P = 0.007). Cx I (enriched in inhibitory terminals) was decreased 33% in schizophrenia (26% in schizophrenia/nonsuicide, 42% in schizophrenia/suicide) and 27% in major depression. Cx II (enriched in excitatory terminals) was not significantly different. Analysis of the ratio of Cx II/Cx I was carried out as an indication of the balance of excitatory to inhibitory terminals. A significant difference between groups (ANOVA, F = 6.42, P = 0.005) was observed. The mean value of Cx II/Cx I was significantly increased by 34% in schizophrenia (26% in schizophrenia/nonsuicide and 43% in schizophrenia/suicide) and by 32% in depression compared with control (Student-Newman-Keuls test, P = 0.05). Immunoreactivities of the two complexins were highly correlated in all groups. However, compared with controls and depression, samples from cases with schizophrenia appeared to have relatively less Cx I for similar amounts of Cx II. Immunocytochemical studies of rat frontal cortex after 3 weeks treatment with chlorpromazine, trifluoperazine or haloperidol revealed no differences in complexins, synaptophysin, SNAP-25, syntaxin or VAMP in comparison with animals treated with vehicle. Alterations of complexins may contribute to the molecular substrate for abnormalities of neural connectivity in severe mental disorders.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:issn |
1359-4184
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
7
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
484-92
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| pubmed:dateRevised |
2009-11-19
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| pubmed:meshHeading |
pubmed-meshheading:12082566-Adaptor Proteins, Vesicular Transport,
pubmed-meshheading:12082566-Adult,
pubmed-meshheading:12082566-Aged,
pubmed-meshheading:12082566-Animals,
pubmed-meshheading:12082566-Cause of Death,
pubmed-meshheading:12082566-Depressive Disorder,
pubmed-meshheading:12082566-Humans,
pubmed-meshheading:12082566-Immunohistochemistry,
pubmed-meshheading:12082566-Male,
pubmed-meshheading:12082566-Middle Aged,
pubmed-meshheading:12082566-Nerve Tissue Proteins,
pubmed-meshheading:12082566-Prefrontal Cortex,
pubmed-meshheading:12082566-Rats,
pubmed-meshheading:12082566-Rats, Sprague-Dawley,
pubmed-meshheading:12082566-Reference Values,
pubmed-meshheading:12082566-Regression Analysis,
pubmed-meshheading:12082566-Schizophrenia,
pubmed-meshheading:12082566-Suicide
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| pubmed:year |
2002
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| pubmed:articleTitle |
Altered immunoreactivity of complexin protein in prefrontal cortex in severe mental illness.
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| pubmed:affiliation |
Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada V5Z 1L8.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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