Temperature dependencies of Ca2+ current, Ca2+-activated Cl- current and Ca2+ transients in sensory neurones

We recorded Ca2+ current (I-Ca) and Ca2+-activated Cl- current (I-Cl(Ca)) in isolated chick dorsal root ganglion neurons. At room temperature, I-Cl(Ca) is activated by Ca2+ influx (e.g. I-Ca) or by caffeine-stimulated release of Ca2+ via ryanodine receptors. Warming from room temperature to 37 degrees C increased the amplitude of I-Ca as well as the amplitude and rate of deactivation of I-Cl(Ca) activated by Ca2+ influx. In contrast, the activation of I-Cl(Ca) by caffeine-stimulated release of Ca2+ from intracellular stores abruptly failed between 19 and 28 degrees C. Warming from 22 to 37 degrees C reduced the amplitude of [Ca2+](i) transients (measured with Indo-1) in chick neurons by more than 50% and reduced [Ca2+](i) transients in mouse neurons by more than 40%. We investigated the role of mitochondria in these phenomena using carbonyl cyanide p-(trifluoromethoxy) phenylhydrazone (FCCP) to inhibit mitochondrial Ca2+ uptake. 1-4 mu M FCCP slowed the deactivation of I-Ca-activated I-Cl(Ca) at 20 degrees C and at 36 degrees C, having a greater effect at the higher temperature. In the presence of FCCP, the rate of deactivation of I-Cl(Ca) was relatively insensitive to temperature in this protocol. In contrast, FCCP had little effect on I-Cl(Ca) activated by caffeine at warmer temperatures (> 22 degrees C) but prolonged I-Cl(Ca) at cooler temperatures (< 22 degrees C). Thus, we find that warming reduces the ability of Ca2+ release to raise [Ca2+](i), increases the effect of mitochondria on the deactivation of I-Cl(Ca) if I-Cl(Ca) is activated by Ca2+ influx, and reduces the effect of mitochondria if I-Cl(Ca) is activated by caffeine-stimulated Ca2+ release.