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

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. Th...

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Published in:Neuroscience research 2007-03, Vol.57 (3), p.339-346
Main Authors: Higashida, Haruhiro, Bowden, Sarah E H, Yokoyama, Shigeru, Salmina, Alla, Hashii, Minako, Hoshi, Naoto, Zhang, Jia-Sheng, Knijnik, Rimma, Noda, Mami, Zhong, Zen-Guo, Jin, Duo, Higashida, Kazuhiro, Takeda, Hisashi, Akita, Tenpei, Kuba, Kenji, Yamagishi, Sayaka, Shimizu, Noriaki, Takasawa, Shin, Okamoto, Hiroshi, Robbins, Jon
Format: Article
Language:English
Subjects:
Acetylcholine - metabolism
Acetylcholine - pharmacology
ADP-ribosyl Cyclase - metabolism
ADP-ribosyl Cyclase 1 - genetics
ADP-ribosyl Cyclase 1 - metabolism
Animals
Calcium - metabolism
Calcium Signaling - drug effects
Calcium Signaling - physiology
Cell Line, Tumor
Clone Cells - drug effects
Clone Cells - metabolism
Cyclic ADP-Ribose - metabolism
Humans
Mice
Neurons - drug effects
Neurons - metabolism
Phenotype
Rats
Receptors, Muscarinic - drug effects
Receptors, Muscarinic - metabolism
Signal Transduction - drug effects
Signal Transduction - physiology
Up-Regulation - drug effects
Up-Regulation - physiology
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Summary: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 Ca(2+) concentrations ([Ca(2+)](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 Ca(2+) release was unchanged between control and overexpressed cells. These results indicate that cADPR is an intracellular messenger of Ca(2+) signalling, suggesting that CD38 can contribute to mAChR-cADPR signalling.
ISSN:0168-0102
DOI:10.1016/j.neures.2006.11.008