tailieunhanh - Báo cáo khoa học: Synchronization of Ca2+ oscillations: a coupled oscillator-based mechanism in smooth muscle

Entrained oscillations in Ca 2+ underlie many biological pacemaking phe-nomena. In this article, we review a long-range signaling mechanism in smooth muscle that results in global outcomes of local interactions. Our results are derived from studies of the following: (a) slow-wave depolariza-tions that underlie rhythmic contractions of gastric smooth muscle; | MINIREVIEW Synchronization of Ca2 oscillations a coupled oscillator-based mechanism in smooth muscle Mohammad S. Imtiaz1 Pierre-Yves von der Weid1 and Dirk F. van Helden2 1 Department of Physiology and Pharmacology University of Calgary Alberta Canada 2 Schoolof BiomedicalSciences University of Newcastle Callaghan NSW Australia Keywords Ca2 oscillations Ca2 stores coupled oscillators lymphatics slow waves synchronization Correspondence M. S. Imtiaz Department of Physiology Pharmacology Faculty of Medicine University of Calgary Health Sciences Centre 3330 HospitalDrive NW Calgary Alberta T2N 4N1 Canada Fax 1 403 210 8195 Tel 1 403 210 9838 E-mail mimtiaz@ Received 31 March 2009 revised 11 September 2009 accepted 14 October 2009 doi Entrained oscillations in Ca2 underlie many biological pacemaking phenomena. In this article we review a long-range signaling mechanism in smooth muscle that results in global outcomes of local interactions. Our results are derived from studies of the following a slow-wave depolarizations that underlie rhythmic contractions of gastric smooth muscle and b membrane depolarizations that drive rhythmic contractions of lymphatic smooth muscle. The main feature of this signaling mechanism is a coupled oscillator-based synchronization of Ca2 oscillations across cells that drives membrane potential changes and causes coordinated contractions. The key elements of this mechanism are as follows a the Ca2 releaserefill cycle of endoplasmic reticulum Ca2 stores b Ca2 -dependent modulation of membrane currents c voltage-dependent modulation of Ca2 store release and d cell-cell coupling through gap junctions or other mechanisms. In this mechanism Ca2 stores alter the frequency of adjacent stores through voltage-dependent modulation of store release. This electrochemical coupling is many orders of magnitude stronger than the coupling through diffusion of Ca2 or inositol 1 4 5-trisphosphate and thus provides an