Mechanisms underlying insect chill-coma.
At their critical thermal minimum (CT(min)) insects enter chill-coma, a reversible state where neuromuscular transmission and movement cease. The physiological mechanisms responsible for the insect CT(min) remain poorly understood despite the regular use of chill-coma onset and recovery as a means to assess evolved or acquired variation in low temperature tolerance. In this review, we summarize the use of chill-coma as a metric of thermal tolerance to date, and synthesise current knowledge on the nature and plasticity of lower thermal limits to present probable physiological mechanisms of cold-induced failure. Chill-coma is likely to be driven by an inability to maintain ionic homeostasis through the effects of temperature on ion-motive ATPases, ion channel gating mechanisms, and/or the lipid membrane, leading to a loss of nerve and muscle excitability.
Department of Biology, The University of Western Ontario, London, ON, N6A 5B7, Canada. hmacmil2@uwo.ca
Heath A
HA
Macmillan
Brent J
BJ
Sinclair
D000251:Adenosine Triphosphatases / Q000235:genetics / Q000378:metabolism; D000818:Animals; D003080:Cold Temperature; D019476:Insect Proteins / Q000235:genetics / Q000378:metabolism; D007313:Insecta / Q000235:genetics / Q000502:physiology*; D007473:Ion Channels / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction
D019476:Insect Proteins; D007473:Ion Channels; D000251:Adenosine Triphosphatases