Temperature dependencies of Ca2+ current, Ca(2+)-activated Cl- current and Ca2+ transients in sensory neurones

We recorded Ca2+ current (ICa) and Ca(2+)-activated Cl- current (ICl(Ca)) in isolated chick dorsal root ganglion neurons. At room temperature, ICl(Ca) is activated by Ca2+ influx (e.g. ICa) or by caffeine-stimulated release of Ca2+ via ryanodine receptors. Warming from room temperature to 37 degrees C increased the amplitude of ICa as well as the amplitude and rate of deactivation of ICl(Ca) activated by Ca2+ influx. In contrast, the activation of ICl(Ca) by caffeine-stimulated release of Ca2+ from intracellular stores abruptly failed between 19 and 28 degrees C. Warning 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 microM FCCP slowed the deactivation of ICa-activated ICl(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 ICl(Ca) was relatively insensitive to temperature in this protocol. In contrast, FCCP had little effect on ICl(Ca) activated by caffeine at warmer temperatures (> 22 degrees C) but prolonged ICl(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 ICl(Ca) if ICl(Ca) is activated by Ca2+ influx, and reduces the effect of mitochondria if ICl(Ca) is activated by caffeine-stimulated Ca2+ release.