title: 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.
authors.affiliation: Institut Fédératif des Neurosciences de Lyon, 69677 Bron cedex, France.
authors.forename: M
authors.initials: M
authors.lastname: Bégou
authors.forename: J
authors.initials: J
authors.lastname: Volle
authors.forename: J-B
authors.initials: JB
authors.lastname: Bertrand
authors.forename: P
authors.initials: P
authors.lastname: Brun
authors.forename: D
authors.initials: D
authors.lastname: Job
authors.forename: A
authors.initials: A
authors.lastname: Schweitzer
authors.forename: M
authors.initials: M
authors.lastname: Saoud
authors.forename: T
authors.initials: T
authors.lastname: D'Amato
authors.forename: A
authors.initials: A
authors.lastname: Andrieux
authors.forename: M-F
authors.initials: MF
authors.lastname: Suaud-Chagny
mesh_terms: D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology*; D003071:Cognition / Q000502:physiology*; D005247:Feeding Behavior / Q000502:physiology; D007398:Interpersonal Relations; D007858:Learning / Q000502:physiology; D008297:Male; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D018345:Mice, Knockout; D008869:Microtubule-Associated Proteins / Q000235:genetics* / Q000502:physiology*; D011597:Psychomotor Performance / Q000502:physiology; D021641:Recognition, Psychology / Q000502:physiology; D012559:Schizophrenia / Q000235:genetics*; D012565:Schizophrenic Psychology; D012903:Smell / Q000502:physiology; D012919:Social Behavior; D013028:Space Perception / Q000502:physiology
chemical_list: D014150:Antipsychotic Agents; D008869:Microtubule-Associated Proteins; C491893:Mtap6 protein, mouse