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Journal articles
STOP knockout and NMDA NR1 hypomorphic mice exhibit deficits in sensorimotor gating.
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.
https://www.hal.inserm.fr/inserm-00380197
Contributor : Annie Andrieux <>
Submitted on : Thursday, July 16, 2009 - 5:13:48 PM
Last modification on : Friday, November 6, 2020 - 3:48:47 AM
Long-term archiving on: : Saturday, November 26, 2016 - 8:35:44 AM
Contributor : Annie Andrieux <>
Submitted on : Thursday, July 16, 2009 - 5:13:48 PM
Last modification on : Friday, November 6, 2020 - 3:48:47 AM
Long-term archiving on: : Saturday, November 26, 2016 - 8:35:44 AM