title: Early motor development is abnormal in complexin 1 knockout mice.
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.
authors.affiliation: Department of Pharmacology, University of Cambridge, Tennis Court Road, Cambridge CB2 1PD, UK.
authors.forename: Dervila
authors.initials: D
authors.lastname: Glynn
authors.forename: Rachel J
authors.initials: RJ
authors.lastname: Sizemore
authors.forename: A Jennifer
authors.initials: AJ
authors.lastname: Morton
mesh_terms: D033942:Adaptor Proteins, Vesicular Transport; D000818:Animals; D000831:Animals, Newborn; D001259:Ataxia / Q000235:genetics* / Q000473:pathology* / Q000503:physiopathology; D001522:Behavior, Animal; D001835:Body Weight; D004525:Efferent Pathways / Q000002:abnormalities* / Q000503:physiopathology; D005260:Female; D018507:Gene Expression Regulation, Developmental; D005838:Genotype; D018466:Gravity Sensing; D018737:Hand Strength; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009048:Motor Skills; D009068:Movement; D009419:Nerve Tissue Proteins / Q000235:genetics* / Q000378:metabolism*; D011187:Posture; D011930:Reaction Time; D012021:Reflex, Abnormal
chemical_list: D033942:Adaptor Proteins, Vesicular Transport; D009419:Nerve Tissue Proteins; C095992:complexin I