Cold acclimation increases cold tolerance of chill-susceptible insects and the acclimation response often involves improved organismal ion balance and osmoregulatory function at low temperature. However, the physiological mechanisms underlying plasticity of ion regulatory capacity are largely unresolved. Here we used Ussing chambers to explore the effects of cold exposure on hindgut KCl reabsorption in cold- (11 °C) and warm-acclimated (30 °C) Locusta migratoria. Cooling (from 30 to 10 °C) reduced active reabsorption across recta from warm-acclimated locusts, while recta from cold-acclimated locusts maintained reabsorption at 10 °C. The differences in transport capacity were not linked to major rearrangements of membrane phospholipid profiles. Yet, the stimulatory effect of two signal transduction pathways were altered by temperature and/or acclimation. cAMP-stimulation increased reabsorption in both acclimation groups, with a strong stimulatory effect at 30 °C and a moderate stimulatory effect at 10 °C. cGMP-stimulation also increased reabsorption in both acclimation groups at 30 °C, but their response to cGMP differed at 10 °C. Recta from warm-acclimated locusts, characterised by reduced reabsorption at 10 °C, recovered reabsorption capacity following cGMP-stimulation at 10 °C. In contrast, recta from cold-acclimated locusts, characterised by sustained reabsorption at 10 °C, were unaffected by cGMP-stimulation. Furthermore, cold-exposed recta from warm-acclimated locusts were insensitive to bafilomycin-α1, a V-type H⁺-ATPase inhibitor, whereas this blocker reduced reabsorption across cold-exposed recta from cold-acclimated animals. In conclusion, bafilomycin-sensitive and cGMP-dependent transport mechanism(s) are likely blocked during cold exposure in warm-acclimated animals while preserved in cold-acclimated animals. These may in part explain the large differences in rectal ion transport capacity between acclimation groups at low temperature.

冷驯化提高了对寒冷敏感昆虫的耐寒性，并且驯化响应通常涉及改善低温下的生物离子平衡和渗透调节功能。但是，离子调节能力可塑性的生理机制在很大程度上尚未解决。在这里，我们使用Ussing室来研究冷暴露（11°C）和温热适应（30°C）的南方蝗对后肠KCl重吸收的影响。冷却（从30°C到10°C）会降低热适应蝗虫在直肠上的主动重吸收，而冷适应蝗虫的直肠在10°C下保持重吸收。转运能力的差异与膜磷脂分布的主要重排无关。然而，温度和/或驯化改变了两种信号转导途径的刺激作用。在两个适应组中，cAMP刺激均增加了重吸收，在30°C时有强烈的刺激作用，在10°C时有中度的刺激作用。在30°C时，cGMP刺激在两个适应组中也增加了重吸收，但在10°C时，它们对cGMP的反应有所不同。来自温热蝗虫的直肠，其特征在于在10°C下减少了重吸收，在10°C下刺激了cGMP后恢复了重吸收能力。相反，来自冷适应蝗虫的直肠，其特征在于在10°C下持续吸收，不受cGMP刺激的影响。此外，来自温热蝗虫的冷暴露直肠对V型H型巴氟霉素-α1不敏感⁺ -ATPase抑制剂，而该阻滞剂降低了冷适应动物的冷暴露直肠中的重吸收。总之，在温暖适应的动物中冷暴露期间，对巴氟霉素敏感和依赖cGMP的转运机制很可能被阻断，而在寒冷适应的动物中保留了。这些可以部分解释低温适应组之间直肠离子转运能力的巨大差异。