Skip to Main content Skip to Navigation
Journal articles

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.
Complete list of metadatas

Cited literature [48 references]  Display  Hide  Download

https://www.hal.inserm.fr/inserm-00375621
Contributor : Annie Andrieux <>
Submitted on : Tuesday, June 23, 2009 - 6:08:26 PM
Last modification on : Wednesday, November 4, 2020 - 2:19:46 PM
Long-term archiving on: : Thursday, June 10, 2010 - 8:34:32 PM

Files

inserm-00375621_edited.pdf
Files produced by the author(s)

Identifiers

Collections

Citation

Melina Bégou, Julien Volle, Jean Batiste Bertrand, Philippe Brun, Didier Job, et al.. The stop null mice model for schizophrenia displays [corrected] cognitive and social deficits partly alleviated by neuroleptics.. Neuroscience, Elsevier - International Brain Research Organization, 2008, 157 (1), pp.29-39. ⟨10.1016/j.neuroscience.2008.07.080⟩. ⟨inserm-00375621⟩

Share

Metrics

Record views

636

Files downloads

1099