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Ca 2+ phase waves: a basis for cellular pacemaking and long‐range synchronicity in the guinea‐pig gastric pylorus
Author(s) -
Helden Dirk F.,
Imtiaz Mohammad S.
Publication year - 2003
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.2003.00271.x
Subject(s) - depolarization , biophysics , membrane potential , chemistry , electrophysiology , gap junction , neuroscience , intracellular , anatomy , biology , biochemistry
Ca 2+ imaging and multiple microelectrode recording procedures were used to investigate a slow wave‐like electrical rhythmicity in single bundle strips from the circular muscle layer of the guinea‐pig gastric pylorus. The ‘slow waves’ (SWs) consisted of a pacemaker and regenerative component, with both potentials composed of more elementary events variously termed spontaneous transient depolarizations (STDs) or unitary potentials. STDs and SW pacemaker and regenerative potentials exhibited associated local and distributed Ca 2+ transients, respectively. Ca 2+ transients were often larger in cellular regions that exhibited higher basal Ca 2+ indicator‐associated fluorescence, typical of regions likely to contain intramuscular interstitial cells of Cajal (ICC IM ). The emergence of rhythmicity arose through entrainment of STDs resulting in pacemaker Ca 2+ transients and potentials, events that exhibited considerable spatial synchronicity. Application of ACh to strips exhibiting weak rhythmicity caused marked enhancement of SW synchronicity. SWs and underlying Ca 2+ increases exhibited very high ‘apparent conduction velocities’ (‘CVs’) orders of magnitude greater than for sequentially conducting Ca 2+ waves. Central interruption of either intercellular connectivity or inositol 1,4,5‐trisphosphate receptor (IP 3 R)‐mediated store Ca 2+ release in strips caused SWs at the two ends to run independently of each other, consistent with a coupled oscillator‐based mechanism. Central inhibition of stores required much wider regions of blockade than inhibition of connectivity indicating that stores were voltage‐coupled. Simulations, made using a conventional store array model but now including depolarization coupled to IP 3 R‐mediated Ca 2+ release, predicted the experimental findings. The linkage between membrane voltage and Ca 2+ release provides a means for stores to interact as strongly coupled oscillators, resulting in the emergence of Ca 2+ phase waves and associated pacemaker potentials. This distributed pacemaker triggers regenerative Ca 2+ release and resultant SWs.