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
Rights & PermissionsPrintExport