Defective Motor Behavior and Neural Gene Expression in RIIβ-Protein Kinase A Mutant Mice

摘要: Motor behavior is modulated by dopamine-responsive neurons in the striatum, where dopaminergic signaling uses G-protein-coupled pathways, including those that result activation of cAMP-dependent protein kinase (PKA). The RIIβ isoform PKA highly enriched and targeted disruption gene mice leads to a dramatic reduction total activity this region. Although mutant show typical locomotor responses after acute administration drugs, they display abnormalities two experience-dependent behaviors: training on rotarod task sensitization amphetamine. In addition, amphetamine induction fos absent, basal expression dynorphin mRNA reduced striatum. These results demonstrate motor learning regulation neuronal require PKA, whereas effects drugs are relatively unaffected deficiency.