Overexpression of human CD38/ADP-ribosyl cyclase enhances acetylcholine-induced Ca2+ signalling in rodent NG108-15 neuroblastoma cells

Haruhiro Higashida, Sarah E.H. Bowden, Shigeru Yokoyama, Alla Salmina, Minako Hashii, Naoto Hoshi, Jia Sheng Zhang, Rimma Knijnik, Mami Noda, Zen Guo Zhong, Duo Jin, Kazuhiro Higashida, Hisashi Takeda, Tenpei Akita, Kenji Kuba, Sayaka Yamagishi, Noriaki Shimizu, Shin Takasawa, Hiroshi Okamoto, Jon Robbins

Research output: Contribution to journalArticlepeer-review

10 Citations (Scopus)


The role of cyclic ADP-ribose (cADPR) and its synthetic enzyme, CD38, as a downstream signal of muscarinic acetylcholine receptors (mAChRs) was examined in neuroblastoma cells expressing M1 mAChRs (NGM1). NGM1 cells were further transformed with both wild-type and mutant (C119K/C201E) human CD38. The dual transformed cells exhibited higher cADPR formation than ADPR production and elevated intracellular free Ca2+ concentrations ([Ca2+]i) in response to ACh. These phenotypes were analyzed in detail in a representative CD38 clone. The intracellular cADPR concentration by ACh application was significantly increased by CD38 overexpression. Digital image analysis by a confocal microscopy revealed that topographical distribution of the sites of Ca2+ release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca2+ signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.

Original languageEnglish
Pages (from-to)339-346
Number of pages8
JournalNeuroscience Research
Issue number3
Publication statusPublished - Mar 2007

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)


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