“…Intracellular cADPR concentrations are known to be regulated in many different ways: in one such mechanism, ADP-ribosyl cyclase or CD38 seems to be coupled directly with neurotransmitter or hormone receptors such as muscarinic acetylcholine or metabotropic glutamate receptors via different G proteins on the membrane surface (Higashida et al, 1997(Higashida et al, , 1999(Higashida et al, , 2007; or phosphorylation downstream of the G-protein-coupled receptor signaling pathway (Boittin et al, 2003;Sternfeld et al, 2003). Specifically, the activation of ADP-ribosyl cyclase or CD38 by cyclic GMP-or cyclic AMP-dependent protein kinases has been reported in Aplysia californica (Graeff et al, 1998), LAK cells (Rah et al, 2005) and artery smooth muscle cells (Boittin et al, 2003). However, there have been no previous reports regarding the mechanisms by which ADP-ribosyl cyclase and CD38 are activated after OT receptor stimulation in the hypothalamus, leading to secretion of OT.…”