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The stop null mice model for schizophrenia displays [corrected] cognitive and social deficits partly alleviated by neuroleptics.

Abstract：

:Recently evidence has accumulated that schizophrenia can arise from primary synaptic defects involving structural proteins particularly, microtubule associated proteins. Previous experiments have demonstrated that a STOP (stable tubule only peptide) gene deletion in mice leads to a phenotype mimicking some aspects of positive symptoms classically observed in schizophrenic patients. In the current study, we determined if STOP null mice demonstrate behavioral abnormalities related to the social and cognitive impairments of schizophrenia. Compared with wild-type mice, STOP null mice exhibited deficits in the non-aggressive component of social recognition, short term working memory and social and spatial learning. As described in humans, learning deficits in STOP null mice were poorly sensitive to long term treatment with typical neuroleptics. Since social and cognitive dysfunction have consistently been considered as central features of schizophrenia, we propose that STOP null mice may provide a useful model to understand the neurobiological correlates of social and cognitive defects in schizophrenia and to develop treatments that better target these symptoms.

journal_name

Neuroscience

journal_title

Neuroscience

authors

Bégou M,Volle J,Bertrand JB,Brun P,Job D,Schweitzer A,Saoud M,D'Amato T,Andrieux A,Suaud-Chagny MF

doi

10.1016/j.neuroscience.2008.07.080

subject

Has Abstract

pub_date

2008-11-11 00:00:00

pages

29-39

issue

1

eissn

0306-4522

issn

1873-7544

pii

S0306-4522(08)01173-1

journal_volume

157

pub_type

杂志文章

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