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Review
. 2001 Nov;26(5):395-410.

Animal models of schizophrenia: a critical review

E R Marcotte  1 , D M Pearson, L K Srivastava
Affiliations
Review

Animal models of schizophrenia: a critical review

E R Marcotte et al. J Psychiatry Neurosci. 2001 Nov.

Abstract
in English, French

Current research into schizophrenia has remained highly fragmented, much like the clinical presentation of the disease itself. Differing theories as to the cause and progression of schizophrenia, as well as the heterogeneity of clinical symptoms, have made it difficult to develop a coherent framework suitable for animal modelling. However, a number of limited animal models have been developed to explore various causative theories and to test specific mechanistic hypotheses. Historically, these models have been based on the manipulation of neurotransmitter systems believed to be involved in schizophrenia. In recent years, the emphasis has shifted to targeting relevant brain regions in an attempt to explore potential etiologic hypotheses. The specific animal models developed within these frameworks are described in this review. Emphasis is placed on the critical evaluation of currently available models because these models help to shape the direction of future research.

La recherche en cours sur la schizophrénie demeure très fragmentée, tout comme la manifestation clinique de la maladie même. Comme les théories sur la cause et l'évolution de la schizophrénie diffèrent et compte tenu de l'hétérogénéité des symptômes cliniques, il est difficile d'établir un cadre cohérent qui convient à une modélisation animale. On a toutefois mis au point des modèles animaux limités pour explorer diverses théories relatives aux causes et vérifier des hypothèses mécanistes précises. Sur le plan historique, ces modèles reposent sur la manipulation des systèmes neurotransmetteurs que l'on croit impliqués dans la schizophrénie. Depuis quelques années, on cherche plutôt à cibler des régions pertinentes du cerveau afin d'explorer des hypothèses étiologiques possibles. On décrit dans cette critique les modèles animaux précis mis au point dans le contexte de ces cadres. On met l'accent sur l'évaluation critique des modèles actuellement disponibles parce qu'ils aident à orienter la recherche future.

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References

    1. Woods BT. Is schizophrenia a progressive neurodevelopmental disorder? Toward a unitary pathogenetic mechanism. Am J Psychiatry 1998;155(12):1661-70. - PubMed
    1. Miller R. Schizophrenia as a progressive disorder: relations to EEG, CT, neuropathological and other evidence. Prog Neurobiol 1989;33(1):17-44. - PubMed
    1. Keshavan MS, Anderson S, Pettegrew JW. Is schizophrenia due to excessive synaptic pruning in the prefrontal cortex? The Feinberg hypothesis revisited. J Psychiatr Res 1994;28(3):239-65. - PubMed
    1. DeLisi LE. Is schizophrenia a lifetime disorder of brain plasticity, growth and aging? Schizophr Res 1997;23(2):119-29. - PubMed
    1. Crow TJ. Schizophrenia as failure of hemispheric dominance for language. Trends Neurosci 1997;20(8):339-43. - PubMed

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