Generation and propagation of gastric slow waves.
1. Mechanisms underlying the generation and propagation of gastrointestinal slow wave depolarizations have long been controversial. The present review aims to collate present knowledge on this subject with specific reference to slow waves in gastric smooth muscle. 2. At present, there is strong agreement that interstitial cells of Cajal (ICC) are the pacemaker cells that generate slow waves. What has been less clear is the relative role of primary types of ICC, including the network in the myenteric plexus (ICC-MY) and the intramuscular network (ICC-IM). It is concluded that both ICC-MY and ICC-IM are likely to serve a major role in slow wave generation and propagation. 3. There has been long-standing controversy as to how slow waves 'propagate' circumferentially and down the gastrointestinal tract. Two mechanisms have been proposed, one being action potential (AP)-like conduction and the other phase wave-based 'propagation' resulting from an interaction of coupled oscillators. Studies made on single bundle gastric strips indicate that both mechanisms apply with relative dominance depending on conditions; the phase wave mechanism is dominant under circumstances of rhythmically generating slow waves and the AP-like propagation is dominant when the system is perturbed. 4. The phase wave mechanism (termed Ca(2+) phase wave) uses cyclical Ca(2+) release as the oscillator, with coupling between oscillators mediated by several factors, including: (i) store-induced depolarization; (ii) resultant electrical current flow/depolarization through the pacemaker cell network; and (iii) depolarization-induced increase in excitability of downstream Ca(2+) stores. An analogy is provided by pendulums in an array coupled together by a network of springs. These, when randomly activated, entrain to swing at the same frequency but with a relative delay along the row giving the impression of a propagating wave. 5. The AP-like mechanism (termed voltage-accelerated Ca(2+) wave) propagates sequentially like a conducting AP. However, it is different in that it depends on regenerative store Ca(2+) release and resultant depolarization rather than regenerative activation of voltage-dependent channels in the cell membrane. 6. The applicability of these mechanisms to describing propagation in large intact gastrointestinal tissues, where voltage-dependent Ca(2+) entry is also likely to be functional, is discussed.
van Helden
Dirk F
DF
School of Biomedical Sciences, Faculty of Health, University of Newcastle, Callaghan, New South Wales, Australia. dirk.vanhelden@newcastle.edu.au
Laver
Derek R
DR
Holdsworth
John
J
Imtiaz
Mohammad S
MS
D000818:Animals; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling / Q000187:drug effects; D006801:Humans; D056885:Interstitial Cells of Cajal / Q000187:drug effects / Q000502:physiology; D008954:Models, Biological; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009130:Muscle, Smooth / Q000187:drug effects / Q000294:innervation; D009197:Myenteric Plexus / Q000502:physiology; D009431:Neural Conduction / Q000187:drug effects; D010528:Peristalsis / Q000187:drug effects / Q000502:physiology*; D013270:Stomach / Q000187:drug effects / Q000294:innervation* / Q000502:physiology*
D002118:Calcium