Abstract
The effects of temperature on the generation of pacemaker potentials recorded from myenteric interstitial cells of Cajal (ICC-MY) distributed in the mouse small intestine were investigated using intracellular recording techniques. In response to increasing temperatures in the range of 26-40 degrees C, the frequency and maximum rate of rise (dV/dt (max)) of pacemaker potentials were increased while their duration was decreased. The resting membrane potential and amplitude of the pacemaker potentials were not affected by change in temperature. Elevation of temperature decreased the amplitude, duration, and rise time of unitary potentials generated spontaneously during intervals between the pacemaker potentials. Metabolic inhibition (KCN and iodoacetic acid) decreased the frequency of pacemaker potentials with no alteration to the amplitude and dV/dt (max). Cyclopiazonic acid (3 muM), an inhibitor of the internal Ca(2+) pump, abolished pacemaker potentials in low-temperature conditions (<29 degrees C) but not at high-temperature conditions (>38 degrees C). These results suggest that the primary and plateau components of pacemaker potentials have different temperature sensitivities: the primary component is highly temperature-sensitive and is activated at higher temperatures, while the plateau component is formed by activation of temperature-insensitive mechanisms. The results also suggest that the mitochondria-induced intracellular Ca(2+) handling system seems to be involved in the initiation of the generation of pacemaker potentials but not in their configuration.
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