抄録
Cyclic ADP-ribose (cADPR) is an endogenous modulator of ryanodine receptor Ca2+ releasing channels in the nervous system. Injection of cADPR into neuronal cells primarily induces a transient Cyclic ADP-ribose (cADPR) is an endogenous modulator of ryanodine receptor Ca2+ releasing channels in the nervous system. Injection of cADPR into neuronal cells primarily induces a transient elevation of intracellular calcium concentration, and/or secondarily potentiates cytosolic calcium increases that are the result of depolarization-induced calcium influx through voltage-activated calcium channels. Acetylcholine release from cholinergic neurons is facilitated by cADPR. cADPR modifies potassium currents, including KCNQ/M channels, rather by a calcium-independent fashion. cADPR is synthesized by both membrane-bound and cytosolic forms of ADP-ribosyl cyclase in neuronal cells. cADPR hydrolase activity is weak in the membrane fraction, but high in the cytoplasm. Stimulation of muscarinic and beta-adrenergic receptors activates membrane-bound ADP-ribosyl cyclase via G proteins within membranes of neuronal tumor cells and cortical astrocytes, as in cardiac myocytes by beta-adrenergic receptors. These results suggest that cADPR might be involved in M1-muscarinic inhibition of both KCNQ2/3 and merg1 channel, and that cADPR is a second messenger in calcium and non-calcium signalings in the nervous system. [Jpn J Physiol 54 Suppl:S18 (2004)]
