Early motor development is abnormal in complexin 1 knockout mice

被引:32
|
作者
Glynn, Dervila [1 ]
Sizemore, Rachel J. [1 ]
Morton, A. Jennifer [1 ]
机构
[1] Univ Cambridge, Dept Pharmacol, Cambridge CB2 1PD, England
关键词
motor; sensory; development; autism; schizophrenia; posture; coordination; cerebellum; test battery; Huntington's disease; JERUSALEM INFANT DEVELOPMENT; SYNAPTIC VESICLE EXOCYTOSIS; MESSENGER-RNA EXPRESSION; SNARE COMPLEX; NEUROBEHAVIORAL DEVELOPMENT; NEUROTRANSMITTER RELEASE; PREFRONTAL CORTEX; MUTANT MICE; SCHIZOPHRENIA; ATAXIA;
D O I
10.1016/j.nbd.2006.10.011
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Complexin I expression is dysregulated in a number of neurological diseases including schizophrenia and depression. Adult complexin 1 knockout (Cplx1(-/-)) mice are severely ataxic and show deficits in exploration and emotional reactivity. Here, we evaluated early behavioural development of Cplx1(-/-) mice. Cplx1(-/-) mice showed marked abnormalities. They develop ataxia by post-natal day 7 (P7), and by P21 show marked deficits in tasks requiring postural skills and complex movement. These deficits are consistent with abnormalities in sensory and motor development found in infants that develop schizophrenia in later life. A role for complexin I depletion should be considered in diseases where deficits in early sensory and motor development exist, such as autism and schizophrenia. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:483 / 495
页数:13
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