@article{oai:kanazawa-u.repo.nii.ac.jp:00030980,
 author = {Higashida, Haruhiro and Salmina, Alla B. and Olovyannikova, Raissa Ya and Hashii, Minako and Yokoyama, Shigeru and Koizumi, Keita and Jin, Duo and Liu, Hong-Xiang and Lopatina, Olga and Amina, Sarwat and Mohammad, Saharul Islam and Huang, Jian-Jun and Noda, Mami},
 issue = {2-4 SPEC. ISS.},
 journal = {Neurochemistry International},
 month = {Jul},
 note = {β-NAD+ is as abundant as ATP in neuronal cells. β-NAD+ functions not only as a coenzyme but also as a substrate. β-NAD+-utilizing enzymes are involved in signal transduction. We focus on ADP-ribosyl cyclase/CD38 which synthesizes cyclic ADP-ribose (cADPR), a universal Ca2+ mobilizer from intracellular stores, from β-NAD+. cADPR acts through activation/modulation of ryanodine receptor Ca2+ releasing Ca2+ channels. cADPR synthesis in neuronal cells is stimulated or modulated via different pathways and various factors. Subtype-specific coupling of various neurotransmitter receptors with ADP-ribosyl cyclase confirms the involvement of the enzyme in signal transduction in neurons and glial cells. Moreover, cADPR/CD38 is critical in oxytocin release from the hypothalamic cell dendrites and nerve terminals in the posterior pituitary. Therefore, it is possible that pharmacological manipulation of intracellular cADPR levels through ADP-ribosyl cyclase activity or synthetic cADPR analogues may provide new therapeutic opportunities for treatment of neurodevelopmental disorders. © 2007., 金沢大学大学院医学系研究科脳細胞分子学},
 pages = {192--199},
 title = {Cyclic ADP-ribose as a universal calcium signal molecule in the nervous system},
 volume = {51},
 year = {2007}
}