Gastrointestinal (GI) motility is well organized. GI muscles act as a functional syncytium to achieve physiological functions under the control of neurones and pacemaker cells, which generate basal spontaneous pacemaker electrical activity. To date, it is unclear how spontaneous electrical activities are coupled, especially within a micrometre range. Here, using a microelectrode array, we show a spatio-temporal analysis of GI spontaneous electrical activity. The muscle preparations were isolated from guinea-pig stomach, and fixed in a chamber with an array of 8 × 8 planar multielectrodes (with 300 μm in interpolar distance). The electrical activities (field potentials) were simultaneously recorded through a multichannel amplifier system after high-pass filtering at 0.1 Hz. Dihydropyridine Ca 2+ channel antagonists are known to differentiate the electrical pacemaker activity of interstitial cells of Cajal (ICCs) by suppressing smooth muscle activity. In the presence of nifedipine, we observed spontaneous electrical activities that were well synchronized over the array area, but had a clear phase shift depending on the distance. The additional application of tetrodotoxin (TTX) had little effect on the properties of the electrical activity. Furthermore, by constructing field potential images, we visualized the synchronization of pacemaker electrical activities resolving phase shifts that were measurable over several hundred micrometres. The results imply a phase modulation mechanism other than neural activity, and we postulate that this mechanism enables smooth GI motility. In addition, some preparations clearly showed plasticity of the pacemaker phase shift.

1 In circular muscle strips of the antrum of guinea-pig stomach, the effects of cromakalim were studied on mechanical activity and intracellular membrane potential.2 Cromakalim inhibited mechanical activity at concentrations higher than 1 .tM, accompanied by membrane hyperpolarization and a decrease in membrane resistance. The hyperpolarization was markedly potentiated in K+-free solution and was still observed in the absence of Na+. 3 Slow wave electrical activity was relatively resistant to cromakalim. Changes in its amplitude and frequency were not consistent but blockade of slow waves was never observed. In many preparations cromakalim induced spike-like potentials at the top of slow waves, or when spike-like potentials already existed they were potentiated. However, mechanical activity was always inhibited. 4 Inhibition by cromakalim of the phasic contractions associated with the slow waves, could not be reversed by increasing the external K+ concentration (12-30 mM). 5 The results suggest that in guinea-pig stomach muscle mechanical suppression by cromakalim does not simply result from membrane hyperpolarization or from inhibition of slow waves. A clear dissociation was found between the mechanical and electrical activities. Slow waves, particularly their frequency, are relatively insensitive to membrane hyperpolarization.