RT Journal Article SR Electronic T1 Defective Motor Behavior and Neural Gene Expression in RIIβ-Protein Kinase A Mutant Mice JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 3639 OP 3649 DO 10.1523/JNEUROSCI.18-10-03639.1998 VO 18 IS 10 A1 Eugene P. Brandon A1 Sheree F. Logue A1 Monique R. Adams A1 Ming Qi A1 Sean P. Sullivan A1 Alvin M. Matsumoto A1 Daniel M. Dorsa A1 Jeanne M. Wehner A1 G. Stanley McKnight A1 Rejean L. Idzerda YR 1998 UL http://www.jneurosci.org/content/18/10/3639.abstract AB Motor behavior is modulated by dopamine-responsive neurons in the striatum, where dopaminergic signaling uses G-protein-coupled pathways, including those that result in the activation of cAMP-dependent protein kinase (PKA). The RIIβ isoform of PKA is highly enriched in the striatum, and targeted disruption of the RIIβ gene in mice leads to a dramatic reduction in total PKA activity in this region. Although the mutant mice show typical locomotor responses after acute administration of dopaminergic drugs, they display abnormalities in two experience-dependent locomotor behaviors: training on the rotarod task and locomotor sensitization to amphetamine. In addition, amphetamine induction of fos is absent, and the basal expression of dynorphin mRNA is reduced in the striatum. These results demonstrate that motor learning and the regulation of neuronal gene expression require RIIβ PKA, whereas the acute locomotor effects of dopaminergic drugs are relatively unaffected by this PKA deficiency.