Why do insects enter and recover from chill coma? Low temperature and high extracellular potassium compromise muscle function in Locusta migratoria

When exposed to low temperatures, many insect species enter a reversible comatose state (chill coma), which is driven by a failure of neuromuscular function. Chill coma and chill coma recovery have been associated with a loss and recovery of ion homeostasis (particularly extracellular [K(+)], [K(+)]...

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Veröffentlicht in:Journal of experimental biology 2014-04, Vol.217 (Pt 8), p.1297-1306
Hauptverfasser: Findsen, Anders, Pedersen, Thomas Holm, Petersen, Asbjørn Graver, Nielsen, Ole Bækgaard, Overgaard, Johannes
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container_end_page 1306
container_issue Pt 8
container_start_page 1297
container_title Journal of experimental biology
container_volume 217
creator Findsen, Anders
Pedersen, Thomas Holm
Petersen, Asbjørn Graver
Nielsen, Ole Bækgaard
Overgaard, Johannes
description When exposed to low temperatures, many insect species enter a reversible comatose state (chill coma), which is driven by a failure of neuromuscular function. Chill coma and chill coma recovery have been associated with a loss and recovery of ion homeostasis (particularly extracellular [K(+)], [K(+)]o) and accordingly onset of chill coma has been hypothesized to result from depolarization of membrane potential caused by loss of ion homeostasis. Here, we examined whether onset of chill coma is associated with a disturbance in ion balance by examining the correlation between disruption of ion homeostasis and onset of chill coma in locusts exposed to cold at varying rates of cooling. Chill coma onset temperature changed maximally 1°C under different cooling rates and marked disturbances of ion homeostasis were not observed at any of the cooling rates. In a second set of experiments, we used isolated tibial muscle to determine how temperature and [K(+)]o, independently and together, affect tetanic force production. Tetanic force decreased by 80% when temperature was reduced from 23°C to 0.5°C, while an increase in [K(+)]o from 10 mmol l(-1) to 30 mmol l(-1) at 23°C caused a 40% reduction in force. Combining these two stressors almost abolished force production. Thus, low temperature alone may be responsible for chill coma entry, rather than a disruption of extracellular K(+) homeostasis. As [K(+)] also has a large effect on tetanic force production, it is hypothesized that recovery of [K(+)]o following chill coma could be important for the time to recovery of normal neuromuscular function.
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Here, we examined whether onset of chill coma is associated with a disturbance in ion balance by examining the correlation between disruption of ion homeostasis and onset of chill coma in locusts exposed to cold at varying rates of cooling. Chill coma onset temperature changed maximally 1°C under different cooling rates and marked disturbances of ion homeostasis were not observed at any of the cooling rates. In a second set of experiments, we used isolated tibial muscle to determine how temperature and [K(+)]o, independently and together, affect tetanic force production. Tetanic force decreased by 80% when temperature was reduced from 23°C to 0.5°C, while an increase in [K(+)]o from 10 mmol l(-1) to 30 mmol l(-1) at 23°C caused a 40% reduction in force. Combining these two stressors almost abolished force production. Thus, low temperature alone may be responsible for chill coma entry, rather than a disruption of extracellular K(+) homeostasis. 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source MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection; Company of Biologists
subjects Animals
Cold Temperature
Extracellular Space - metabolism
Female
Homeostasis
Locusta migratoria - physiology
Male
Membrane Potentials
Musculoskeletal Physiological Phenomena
Potassium - metabolism
Water-Electrolyte Balance
title Why do insects enter and recover from chill coma? Low temperature and high extracellular potassium compromise muscle function in Locusta migratoria
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