Specific Ca2+ signaling evoked by cholecystokinin and acetylcholine: the roles of NAADP, cADPR, and IP3.
In order to control cell functions, hormones and neurotransmitters generate an amazing diversity of Ca2+ signals such as local and global Ca2+ elevations and also Ca2+ oscillations. In pancreatic acinar cells, cholecystokinin (CCK) stimulates secretion of digestive enzyme and promotes cell growth, whereas acetylcholine (ACh) essentially triggers enzyme secretion. Pancreatic acinar cells are a classic model for the study of CCK- and ACh-evoked specific Ca2+ signals. In addition to inositol 1,4,5 trisphosphate (IP3), recent studies have shown that cyclic ADPribose (cADPr) and nicotinic acid adenine dinucleotide phosphate (NAADP) release Ca2+ in pancreatic acinar cells. Moreover, it has also been shown that both ACh and CCK trigger Ca2+ spikes by co-activation of IP3 and ryanodine receptors but by different means. ACh uses IP3 and Ca2+, whereas CCK uses cADPr and NAADP. In addition, CCK activates phospholipase A2 and D. The concept emerging from these studies is that agonist-specific Ca2+ signals in a single target cell are generated by combination of different intracellular messengers.
Cancela
J M
JM
MRC Secretory Control Research Group, The Physiological Laboratory, University of Liverpool, Liverpool L69 3BX, UK. j.m.cancela@liverpool.ac.uk
D000109:Acetylcholine / Q000502:physiology*; D000246:Adenosine Diphosphate Ribose / Q000031:analogs & derivatives / Q000502:physiology*; D000818:Animals; D020013:Calcium Signaling / Q000502:physiology*; D002766:Cholecystokinin / Q000502:physiology*; D036563:Cyclic ADP-Ribose; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000502:physiology; D009249:NADP / Q000031:analogs & derivatives / Q000502:physiology*
D036563:Cyclic ADP-Ribose; D000246:Adenosine Diphosphate Ribose; D009249:NADP; C024376:NAADP; D015544:Inositol 1,4,5-Trisphosphate; D002766:Cholecystokinin; D000109:Acetylcholine