作者: Aline L. M. Campana , Laure Rondi-Reig , Christine Tobin , Ann M. Lohof , Florence Picquet
DOI: 10.1046/J.1460-9568.2003.02631.X
关键词:
摘要: We have combined genetic and pharmacological approaches to investigate the behavioural consequences of inactivation murine p53 protein. Our analysis revealed that p53-null mice (p53KO) exhibit a very specific significant motor deficit in rapid walking synchronization. This deficit, observed using rotarod test, was only defect p53KO mice. demonstrated it not due an increase neuronal number or abnormal connectivity olivo-cerebellar system, thought control In order test role central nervous we injected inhibitor activation, pifithrin-a, into cerebellum wild-type treatment mimicked synchronization mice, suggesting presence protein is necessary execute this walking. investigation reveals functional cerebellar adult