抄録
Rap1A, first identified as a suppressor of transformed phenotype was induced by an activated ras oncogene. Like Ras, Rap1A is abundantly expressed in the brain. Perturbation of Ras signaling in mammals results in various neural phenotypes including unstable LTP and deficit in cognition, memory consolidation and spatial learning. The neurophysiological function of Rap1A, however, is poorly understood. Effects of Rap1 and Ras, on the sodium channel activity were studied using sindbis virus-mediated gene transfer. We have found that 1) Rap1A suppresses action potential generation 2) Rap1A suppressed the enhancing sodium current by high level of cAMP, whereas Ras suppressed the reducing sodium current by low level of cAMP. 3) The effects on sodium current were prevented by specific PKA inhibitor. These results suggest that Rap1A serve as a counteracting molecule of Ras in neuronal functions and regulate cAMP dependent cellular signaling mechanisms. [Jpn J Physiol 55 Suppl:S44 (2005)]
