Cold-acclimation increases depolarization resistance and tolerance in muscle fibers from a chill-susceptible insect, Locusta migratoria

Cold exposure depolarizes cells in insects due to a reduced electrogenic ion transport and a gradual increase in extracellular [K+]. Cold-induced depolarization is linked to cold injury in chill-susceptible insects, and the locust, Locusta migratoria, has shown improved cold tolerance following cold-acclimation through depolarization resistance. Here we investigate how cold-acclimation influences depolarization resistance and how this resistance relates to improved cold tolerance. To address this question, we investigated if cold-acclimation affects the electrogenic transport capacity and/or the relative K+ permeability during cold exposure by measuring membrane potentials of warm- and cold-acclimated locusts in the presence/absence of ouabain (Na+/K+ pump blocker) or 4-aminopyridine (4-AP, voltage-gated K+ channel blocker). In addition, we compared the membrane lipid composition of muscle tissue from warm- and cold-acclimated locust, and the abundance of a range transcripts related to ion transport and cell injury accumulation. We found that cold-acclimated locusts are depolarization resistant due to an elevated K+ permeability, facilitated by opening of 4-AP sensitive K+ channels. In accordance, cold-acclimation was associated with an increased abundance of shaker transcripts (gene encoding 4-AP sensitive voltage-gated K+ channels). Furthermore, we found that cold-acclimation improved muscle cell viability following exposure to cold and hyperkalemia even when muscles were depolarized substantially. Thus, cold-acclimation confers resistance to depolarization by altering the relative ion permeability, but cold-acclimated locusts are also more tolerant to depolarization.

Methods
Methods are described in the associated article