Mice lacking p35 display hyperactivity and paradoxical response to psychostimulants.

摘要: Cyclin-dependent kinase 5/p35 complex plays a critical role in dopaminergic neurotransmission. Dysregulation of dopamine (DA) signaling is associated with neurological and neuropsychiatric disorders. As cyclin-dependent 5 (Cdk5) requires association p35 for its proper activation, we hypothesized that dysregulation Cdk5 activity might have an effect on striatal-mediated behavior. We used mutant mouse, deficient protein (p35 KO), which displayed reduced activity. Throughout behavioral biochemical characterization naive psychostimulant-treated mice, demonstrated only juvenile KO mice spontaneous hyperactivity, responded paradoxical hypolocomotor to psychostimulant drugs exhibited deficit inhibition. Strong immunolabeling tyrosine-hydroxylase high striatal DA synthesis contents low turnover, were reverted by psychostimulants, also found mice. Our results demonstrate deficiency critically involved the expression hyperactive phenotype hyper-functioning system, emphasizing importance normal motor emotional features. Thus, may be another useful animal model understanding cellular molecular events underlying attention hyperactivity disorder-like