Department of Biology, The University of Western Ontario, London, ON, N6A 5B7, Canada.
J Insect Physiol. 2011 Jan;57(1):12-20. doi: 10.1016/j.jinsphys.2010.10.004. Epub 2010 Oct 27.
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.
在其临界热最小值 (CT(min))时，昆虫进入冷昏迷状态，这是一种神经肌肉传递和运动停止的可逆状态。尽管经常使用冷昏迷的开始和恢复作为评估低温耐受性的进化或获得变异的手段，但负责昆虫 CT(min)的生理机制仍知之甚少。在这篇综述中，我们总结了迄今为止使用冷昏迷作为热耐受性指标的情况，并综合了目前关于较低热极限的性质和可塑性的知识，以提出冷诱导失效的可能生理机制。冷昏迷可能是由于温度对离子动力 ATP 酶、离子通道门控机制和/或脂质膜的影响，导致无法维持离子动态平衡，从而导致神经和肌肉兴奋性丧失。
