Phosphorylation and inhibition of olfactory adenylyl cyclase by CaM kinase II in Neurons: a mechanism for attenuation of olfactory signals.

摘要: Acute desensitization of olfactory signaling is a critical property the system that allows animals to detect and respond odorants. Correspondingly, an important feature odorant-stimulated cAMP increases their transient nature, phenomenon may be attributable unique regulatory properties adenylyl cyclase (AC3). AC3 stimulated by receptor activation inhibited Ca2+ through Ca2+/calmodulin kinase II (CaMKII) phosphorylation at Ser-1076. Since are accompanied elevated intracellular Ca2+, CaMKII inhibition contribute termination signaling. To test this hypothesis, we generated polyclonal antibody specific for phosphorylated A brief exposure mouse cilia or primary neurons odorants This was blocked inhibitors CaMKII, which also ablated decreases associated with transients. These data define novel mechanism in responses.