Indexed on: 07 Jun '14Published on: 07 Jun '14Published in: The Journal of experimental biology
Insects enter chill coma, a reversible state of paralysis, at temperatures below their critical thermal minimum (CTmin), and the time required for an insect to recover after a cold exposure is termed chill coma recovery time (CCRT). The CTmin and CCRT are both important metrics of insect cold tolerance that are used interchangeably, although chill coma recovery is not necessarily permitted by a direct reversal of the mechanism causing chill coma onset. Nevertheless, onset and recovery of coma have been attributed to loss of neuromuscular function due to depolarization of muscle fibre membrane potential (Vm). Here we test the hypothesis that muscle depolarization at chill coma onset and repolarization during chill coma recovery are caused by changes in extracellular [K(+)] and/or other effects of low temperature. Using Locusta migratoria, we measured in vivo muscle resting potentials of the extensor tibialis during cooling, following prolonged exposure to -2°C and during chill coma recovery, and related changes in Vm to transmembrane [K(+)] balance and temperature. Although Vm was rapidly depolarized by cooling, hemolymph [K(+)] did not rise until locusts had spent considerable time in the cold. Nonetheless, a rise in hemolymph [K(+)] during prolonged cold exposure further depressed muscle resting potential and slowed recovery from chill coma upon rewarming. Muscle resting potentials had a bimodal distribution, and with elevation of extracellular [K(+)] (but not temperature) muscle resting potentials become unimodal. Thus, a disruption of extracellular [K(+)] does depolarize muscle resting potential and slow CCRT following prolonged cold exposure. However, onset of chill coma at the CTmin relates to an as-yet-unknown effect of temperature on neuromuscular function.