Cognitive impairments in the STOP null mouse model of schizophrenia

Abstract

Cognitive dysfunction is a primary and persisting core deficit of schizophrenia that is marginally improved by antipsychotic treatment. Adult mice that lack the stable tubule-only polypeptide (STOP) have neurochemical and behavioral abnormalities that model some features of schizophrenia. Recognition and long-term memory in the STOP null mouse were tested with the novel object recognition task and an olfactory discrimination task, respectively. Researchers examined the brains from STOP null mice to determine whether differences in task performance were associated with alterations in brain morphology. STOP null mice displayed deficits in both recognition and long-term memory. These behavioral deficits were accompanied by a massive enlargement of the cerebral ventricular system as well as by reductions in volume of cortical and diencephalic structures. In addition to deficits in recognition and long-term memory, STOP null mice displayed exaggerated neuroanatomical deficits somewhat reminiscent of those observed among individuals with schizophrenia.