Cold acclimation modulates voltage gated Ca2+ channel currents and fiber excitability in skeletal muscles of Locusta migratoria.

Cold exposure is known to induce stressful imbalances in chill susceptible insects, including loss of hemolymph water, hyperkalemia and cell depolarization. Cold induced depolarization induces uncontrolled Ca2+ influx and accumulation of injury through necrosis/apoptosis. Conversely cold induced Ca2+ influx has been shown to induce rapid cold hardening and therefore also play a role to reduce cold injury. Cold acclimation is known to reduce cold injury in insects and due to the involvement of depolarization and Ca2+ in the pathophysiology of hypothermia, we hypothesized that cold acclimation modulates voltage gated Ca2+ channels and fiber excitability. Using intracellular electrodes or force transducers, we measured the Ca2+ currents, fiber excitability and muscle contractility in warm (31 °C) and cold (11 °C) acclimated locusts. Experiments were performed under conditions ranging from mild conditions where the membrane potential is well regulated to stressful conditions, where the membrane potential is very depolarized and the tissue is at risk of accumulating injury. These experiments found that cold acclimation modulates Ca2+ currents and fiber excitability in a manner that depends on the cold exposure. Thus, under mild conditions, Ca2+ currents and fiber excitability was increased whilst muscle contractility was unaffected by cold acclimation. Conversely, fiber excitability and muscle contractility was decreased under stressful conditions. Further work is required to fully understand the adaptive effects of these modulations. However, we propose a model which reconciles the dualistic role of the Ca2+ ion in cold exposure and cold acclimation. Thus, increased Ca2+ currents at mild temperatures could help to enhance cold sensing capacity whereas reduced fiber excitability under stressful conditions could help to reduce catastrophic Ca2+ influx during periods of severe cold exposure.