Abstract
The complex neurodevelopmental disorder schizophrenia is thought to be induced by an interaction between predisposing genes and environmental stressors. In order to get a better insight into the aetiology of this complex disorder, animal models have been developed. In this review, we summarize mRNA expression profiling studies on neurodevelopmental, pharmacological and genetic animal models for schizophrenia. We discuss parallels and contradictions among these studies, and propose strategies for future research.
Keywords: Animal model, behavior, genetics, microarray, mRNA expression, neurodevelopment, pharmacology, Gene Expression, Rodent Models, Schizophrenia, delusions, hallucinations, ganized speech, grossly disorganized, catatonic behaviour, negative symptoms, neuregulin-1, transferase, hyperlocomotion, social withdrawal, loss of prepulse, cognitive deficits, serotonin, Affymetrix, quantitative polymerase chain reaction, astrocytes, hippocampus, cytokine, apoptosis, calcium/calmodulin signaling, neurotransmitter, VH lesions, haloperidol, mitochondrial cytochrome, oxidase, chondrial tRNA, isoforms, adenosine, transthyretin, glutamate, substances, phencyclidine, prefrontal cortex, Leiomodin 2, ketamine, cyclo-oxygenase, NMDA receptor, MK-801
Current Neuropharmacology
Title: Gene Expression Profiling in Rodent Models for Schizophrenia
Volume: 8 Issue: 4
Author(s): Jessica E. Van Schijndel and Gerard J.M. Martens
Affiliation:
Keywords: Animal model, behavior, genetics, microarray, mRNA expression, neurodevelopment, pharmacology, Gene Expression, Rodent Models, Schizophrenia, delusions, hallucinations, ganized speech, grossly disorganized, catatonic behaviour, negative symptoms, neuregulin-1, transferase, hyperlocomotion, social withdrawal, loss of prepulse, cognitive deficits, serotonin, Affymetrix, quantitative polymerase chain reaction, astrocytes, hippocampus, cytokine, apoptosis, calcium/calmodulin signaling, neurotransmitter, VH lesions, haloperidol, mitochondrial cytochrome, oxidase, chondrial tRNA, isoforms, adenosine, transthyretin, glutamate, substances, phencyclidine, prefrontal cortex, Leiomodin 2, ketamine, cyclo-oxygenase, NMDA receptor, MK-801
Abstract: The complex neurodevelopmental disorder schizophrenia is thought to be induced by an interaction between predisposing genes and environmental stressors. In order to get a better insight into the aetiology of this complex disorder, animal models have been developed. In this review, we summarize mRNA expression profiling studies on neurodevelopmental, pharmacological and genetic animal models for schizophrenia. We discuss parallels and contradictions among these studies, and propose strategies for future research.
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Cite this article as:
E. Van Schijndel Jessica and J.M. Martens Gerard, Gene Expression Profiling in Rodent Models for Schizophrenia, Current Neuropharmacology 2010; 8 (4) . https://dx.doi.org/10.2174/157015910793358132
DOI https://dx.doi.org/10.2174/157015910793358132 |
Print ISSN 1570-159X |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6190 |
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