1. Early motor development is abnormal in complexin 1 knockout mice.
- Author
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Glynn D, Sizemore RJ, and Morton AJ
- Subjects
- Adaptor Proteins, Vesicular Transport, Animals, Animals, Newborn, Ataxia physiopathology, Behavior, Animal, Body Weight, Efferent Pathways physiopathology, Female, Gene Expression Regulation, Developmental, Genotype, Gravity Sensing, Hand Strength, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Motor Skills, Movement, Posture, Reaction Time, Reflex, Abnormal, Ataxia genetics, Ataxia pathology, Efferent Pathways abnormalities, Nerve Tissue Proteins genetics, Nerve Tissue Proteins metabolism
- Abstract
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.
- Published
- 2007
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