Source:http://linkedlifedata.com/resource/pubmed/id/17329300
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2007-3-1
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| pubmed:abstractText |
Acute administration of the psychotomimetic phencyclidine (PCP) can mimic some features of schizophrenia, while a repeated treatment regimen of PCP may provide a more effective way to model in animals the enduring cognitive dysfunction observed in many schizophrenic patients. The present study aims to investigate behavioural and neuropathological effects of sub-chronic PCP administration. The cognitive deficit induced by sub-chronic PCP was examined using a previously established operant reversal-learning paradigm. Subsequently, the effect of sub-chronic PCP on parvalbumin-immunoreactive (parvalbumin-IR) neurons was assessed using immunohistochemical techniques. Rats were trained to respond for food in an operant reversal-learning paradigm for approximately 6 weeks, followed by sub-chronic administration of PCP (2mg/kg) or vehicle twice daily for 7 days followed 7 days later by behavioural testing. Six weeks post PCP, brains were analysed using immunohistochemical techniques to determine the size and density of parvalbumin-IR in the frontal cortex and hippocampus. Sub-chronic PCP significantly reduced (p <0.001) percentage correct responding in the reversal phase relative to the initial phase, an effect that persisted throughout the experimental period (4 weeks). The density of parvalbumin-IR neurons was reduced in the hippocampus, with significant reductions in the dentate gyrus and CA2/3 regions (p <0.001). There were significant changes in the frontal cortex, with a reduction (p <0.01) in the M1 (motor area 1) region and increases in the M2 (motor area 2) region and cingulate cortex (p <0.01-p <0.001). These results parallel findings of profound hippocampal and more subtle cortical deficits of parvalbumin-IR neurons in schizophrenia, and provide evidence to suggest that sub-chronic PCP can induce a lasting cognitive deficit, an effect that may be related to the observed neuronal deficits.
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| pubmed:commentsCorrections | |
| 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:month |
Mar
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| pubmed:issn |
0269-8811
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
21
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
198-205
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| pubmed:dateRevised |
2008-9-25
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| pubmed:meshHeading |
pubmed-meshheading:17329300-Animals,
pubmed-meshheading:17329300-Behavior, Animal,
pubmed-meshheading:17329300-Cognition Disorders,
pubmed-meshheading:17329300-Conditioning, Operant,
pubmed-meshheading:17329300-Dentate Gyrus,
pubmed-meshheading:17329300-Disease Models, Animal,
pubmed-meshheading:17329300-Female,
pubmed-meshheading:17329300-Hallucinogens,
pubmed-meshheading:17329300-Hippocampus,
pubmed-meshheading:17329300-Immunohistochemistry,
pubmed-meshheading:17329300-Interneurons,
pubmed-meshheading:17329300-Parvalbumins,
pubmed-meshheading:17329300-Phencyclidine,
pubmed-meshheading:17329300-Prefrontal Cortex,
pubmed-meshheading:17329300-Rats,
pubmed-meshheading:17329300-Reversal Learning,
pubmed-meshheading:17329300-Schizophrenia,
pubmed-meshheading:17329300-gamma-Aminobutyric Acid
|
| pubmed:year |
2007
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| pubmed:articleTitle |
Sub-chronic psychotomimetic phencyclidine induces deficits in reversal learning and alterations in parvalbumin-immunoreactive expression in the rat.
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| pubmed:affiliation |
Bradford School of Pharmacy, University of Bradford, Bradford, UK.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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