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• W1965118964 abstract "Schizophrenia is a chronic and debilitating disease which is thought to arise from a neuro-developmental disorder. Both the stable tubule-only polypeptide (STOP) protein and the N-methyl-d-aspartate (NMDA) NR1 subunit are involved in neuronal development and physiology. It has therefore been postulated that transgenic mice lacking either the STOP or the NMDAR1 gene would show a ‘schizophrenic-like’ phenotype. Here, STOP knockout and NMDA NR1 hypomorphic mice were assessed in a behavioural measure that can be used to detect schizophrenic-like phenotypes: a change in sensorimotor gating, measured through prepulse inhibition (PPI). STOP knockout mice were further assessed in another measure of ‘schizophrenic-like behaviour’: hyperlocomotion. The PPI deficit exhibited by both the STOP knockout and NMDA knockdown mice could not be reversed by acute treatment with the atyptical antipsychotic, clozapine (1 mg/kg, i.p.) but the hyperlocomotion shown by the STOP knockout mice was reversed with the same acute dose of clozapine." @default.
• W1965118964 created "2016-06-24" @default.
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• W1965118964 date "2005-09-01" @default.
• W1965118964 modified "2023-09-27" @default.
• W1965118964 title "STOP knockout and NMDA NR1 hypomorphic mice exhibit deficits in sensorimotor gating" @default.
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• W1965118964 doi "https://doi.org/10.1016/j.bbr.2005.05.012" @default.
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