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Animal models of schizophrenia
Jones, CA ; Watson, DJG ; Fone, KCF
British journal of pharmacology, 2011-10, Vol.164 (4), p.1162-1194
[Periódico revisado por pares]
Oxford, UK: Blackwell Publishing Ltd
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Título:
Animal models of schizophrenia
Autor:
Jones, CA
;
Watson, DJG
;
Fone, KCF
Assuntos:
Amphetamine - pharmacology
;
Amphetamine - therapeutic use
;
animal model
;
Animals
;
Antipsychotic Agents - pharmacology
;
Antipsychotic Agents - therapeutic use
;
antipsychotics
;
Cognition Disorders - diagnosis
;
Cognition Disorders - drug therapy
;
Cognition Disorders - metabolism
;
Cognition Disorders - psychology
;
DISC‐1
;
Disease Models, Animal
;
dysbindin
;
Female
;
Humans
;
isolation rearing
;
Male
;
Medical research
;
Mice
;
Models, Genetic
;
Models, Neurological
;
neuregulin
;
Neuropsychological Tests
;
phencyclidine
;
Psychotropic drugs
;
Rats
;
reelin
;
Reviews
;
Schizophrenia
;
Schizophrenia - diagnosis
;
Schizophrenia - drug therapy
;
Schizophrenia - metabolism
;
Schizophrenia - physiopathology
;
ventral hippocampal lesion
É parte de:
British journal of pharmacology, 2011-10, Vol.164 (4), p.1162-1194
Notas:
ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Feature-3
ObjectType-Review-1
Descrição:
Developing reliable, predictive animal models for complex psychiatric disorders, such as schizophrenia, is essential to increase our understanding of the neurobiological basis of the disorder and for the development of novel drugs with improved therapeutic efficacy. All available animal models of schizophrenia fit into four different induction categories: developmental, drug‐induced, lesion or genetic manipulation, and the best characterized examples of each type are reviewed herein. Most rodent models have behavioural phenotype changes that resemble ‘positive‐like’ symptoms of schizophrenia, probably reflecting altered mesolimbic dopamine function, but fewer models also show altered social interaction, and learning and memory impairment, analogous to negative and cognitive symptoms of schizophrenia respectively. The negative and cognitive impairments in schizophrenia are resistant to treatment with current antipsychotics, even after remission of the psychosis, which limits their therapeutic efficacy. The MATRICS initiative developed a consensus on the core cognitive deficits of schizophrenic patients, and recommended a standardized test battery to evaluate them. More recently, work has begun to identify specific rodent behavioural tasks with translational relevance to specific cognitive domains affected in schizophrenia, and where available this review focuses on reporting the effect of current and potential antipsychotics on these tasks. The review also highlights the need to develop more comprehensive animal models that more adequately replicate deficits in negative and cognitive symptoms. Increasing information on the neurochemical and structural CNS changes accompanying each model will also help assess treatments that prevent the development of schizophrenia rather than treating the symptoms, another pivotal change required to enable new more effective therapeutic strategies to be developed. LINKED ARTICLES This article is part of a themed issue on Translational Neuropharmacology. To view the other articles in this issue visit http://dx.doi.org/10.1111/bph.2011.164.issue‐4
Editor:
Oxford, UK: Blackwell Publishing Ltd
Idioma:
Inglês
Links
View this record in MEDLINE/PubMed
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