Reversing sodium differentials between the hemolymph and hindgut speeds chill coma recovery but reduces survival in the fall field cricket, Gryllus pennsylvanicus.

@article{Lebenzon2020ReversingSD,
  title={Reversing sodium differentials between the hemolymph and hindgut speeds chill coma recovery but reduces survival in the fall field cricket, Gryllus pennsylvanicus.},
  author={Jacqueline E. Lebenzon and Lauren E. Des Marteaux and Brent J. Sinclair},
  journal={Comparative biochemistry and physiology. Part A, Molecular \& integrative physiology},
  year={2020},
  pages={
          110699
        }
}
5 Citations
Cold acclimation preserves hindgut reabsorption capacity at low temperature in a chill-susceptible insect, Locusta migratoria.
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The role of the gut in insect chilling injury: cold-induced disruption of osmoregulation in the fall field cricket, Gryllus pennsylvanicus
TLDR
A loss of homeostasis is likely to be a primary mechanism driving the cold-induced loss of muscle excitability and progression of chilling injury in chill-susceptible insect species.
Reestablishment of ion homeostasis during chill-coma recovery in the cricket Gryllus pennsylvanicus
TLDR
Evidence is provided that physiological mechanisms of hemolymph ion content and volume regulation, such as ion-motive ATPase activity, are instrumental in chill-coma recovery and may underlie natural variation in insect cold tolerance.
Rapid cold hardening improves recovery of ion homeostasis and chill coma recovery time in the migratory locust, Locusta migratoria
TLDR
It is indicated that loss and recovery of muscular function are associated with the resting membrane potential of excitable membranes as attested by the changes in the equilibrium potential for K+ (EK) following CS.
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TLDR
Three acclimation groups of the adult bugs Pyrrhocoris apterus differed markedly in their levels of chill tolerance, with the least chill-tolerant insects (LD) showing the highest rate of body-water loss.
Why do insects enter and recover from chill coma? Low temperature and high extracellular potassium compromise muscle function in Locusta migratoria
TLDR
Low temperature alone may be responsible for chill coma entry, rather than a disruption of extracellular K+ homeostasis, and recovery of [K+]o following chill coma could be important for the time to recovery of normal neuromuscular function.
Sodium distribution predicts the chill tolerance of Drosophila melanogaster raised in different thermal conditions.
TLDR
These findings extend earlier observations of hemolymph volume disruption during cold exposure to the most ubiquitous model insect (D. melanogaster), highlight shared mechanisms of developmental and adult thermal plasticity and provide strong support for ionoregulatory failure as a central mechanism of insect chill susceptibility.
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