Flight muscle resting potential and species-specific differences in chill-coma

Hosler, Jay S; Burns, John E.; Esch, Harald

doi:10.1016/s0022-1910(99)00148-1

Cited by 114 publications

(123 citation statements)

References 21 publications

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“…Our results suggest that (temperature-independent) development time may account for some variation in the magnitude of the RCH response, and we suggest that this relationship could well be relevant to individual survival in the field. Badre et al (2005) showed that CO 2 blocks signal transduction at the neuromuscular junction resulting in anesthesia, while the onset of chill coma is thought to result from unexcitable muscle cells due to a loss of function of the Na + /K + ATPase, leading to equilibration of membrane ions and loss of the membrane potential (Goller and Esch, 1990;Hosler et al, 2000). Given that nothing is currently known about the mechanisms of recovery from chill coma or anesthesia in insects, we here tentatively assume that recovery is a simple reversal of these events.…”

Section: Anesthetic Effects On Cold Tolerance and Rchmentioning

confidence: 99%

“…Although the mechanisms of chill coma onset are poorly understood, Goller and Esch (1990) suggest that it results from a loss of function of the ion channels necessary for maintaining the membrane potential, leading to voltage equilibration and a loss of muscle cell excitability. Since resting potentials in insects are mostly maintained by a Na + /K + ATPase (Huddart and Wood, 1966;Rheuben, 1972), Hosler et al (2000) suggest that its activity is temperature dependent, and coordination recovery after return to room temperature is dependent upon functional restoration of this pump. However, the underlying causes of chill coma recovery variation have not been investigated, it is unclear whether the mechanisms are shared with chill coma onset and the mechanisms permitting modification of chill coma recovery are almost certainly different to those involved in RCH or basal cold tolerance (Sinclair and Roberts, 2005).…”

Section: Introductionmentioning

confidence: 99%

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The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

Nilson

Sinclair

Roberts

2006

Journal of Insect Physiology

114

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Carbon dioxide gas is used as an insect anesthetic in many laboratories, despite recent studies which have shown that CO 2 can alter behavior and fitness. We examine the effects of CO 2 and anoxia (N 2 ) on cold tolerance, measuring the rapid cold-hardening (RCH) response and chill coma recovery in Drosophila melanogaster. Short exposures to CO 2 or N 2 do not significantly affect RCH, but 60 min of exposure negates RCH. Exposure to CO 2 anesthesia increases chill coma recovery time, but this effect disappears if the flies are given 90 min recovery in air before chill coma induction. Flies treated with N 2 show a similar pattern, but require significantly longer chill coma recovery times even after 90 min of recovery from anoxia. Our results suggest that CO 2 anesthesia is an acceptable way to manipulate flies before cold tolerance experiments (when using RCH or chill coma recovery as a measure), provided exposure duration is minimized and recovery is permitted before chill coma induction. However, we recommend that exposure to N 2 not be used as a method of anesthesia for chill coma studies.

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Section: Anesthetic Effects On Cold Tolerance and Rchmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

Nilson

Sinclair

Roberts

2006

Journal of Insect Physiology

114

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“…Chill tolerance has been shown to be closely associated with the ability to maintain ion and water balance during cold stress, such that cell membrane potential (V m ) is preserved (Koštál et al, 2004;Zachariassen et al, 2004;MacMillan and Sinclair, 2011a;Overgaard and MacMillan, 2016). When a chill-susceptible insect is gradually cooled, reduced ion pump activity causes the V m of excitable tissues to depolarize, and this depolarization often coincides with the onset of chill coma (Pichon and Treherne, 1974;Wareham et al, 1974;Hosler et al, 2000;Andersen et al, 2015a;Overgaard and MacMillan, 2016). Following chill coma onset, hemolymph ion balance is progressively lost, which further depolarizes V m (MacMillan et al, 2014;Overgaard and MacMillan, 2016).…”

Section: Introductionmentioning

confidence: 99%

Cold-acclimation improves chill tolerance in the migratory locust through preservation of ion balance and membrane potential

Andersen

Folkersen

MacMillan

et al. 2016

Journal of Experimental Biology

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Most insects have the ability to alter their cold tolerance in response to temporal temperature fluctuations, and recent studies have shown that insect cold tolerance is closely tied to the ability to maintain transmembrane ion gradients that are important for the maintenance of cell membrane potential (V m ). Several studies have therefore suggested a link between preservation of V m and cellular survival after cold stress, but none has measured V m in this context. We tested this hypothesis by acclimating locusts (Locusta migratoria) to high (31°C) and low temperature (11°C) for 4 days before exposing them to cold stress (0°C) for up to 48 h and subsequently measuring ion balance, cell survival, muscle V m , and whole animal performance. Cold stress caused gradual muscle cell death, which coincided with a loss of ion balance and depolarization of muscle V m . The loss of ion balance and cell polarization were, however, dampened markedly in cold-acclimated locusts such that the development of chill injury was reduced. To further examine the association between cellular injury and V m we exposed in vitro muscle preparations to cold buffers with low, intermediate, or. These experiments revealed that cellular injury during cold exposure occurs when V m becomes severely depolarized. Interestingly, we found that cellular sensitivity to hypothermic hyperkalaemia was lower in cold-acclimated locusts that were better able to defend V m whilst exposed to high extracellular [K + ]. Together these results demonstrate a mechanism of cold acclimation in locusts that improves survival after cold stress: increased cold tolerance is accomplished by preservation of V m through maintenance of ion homeostasis and decreased K + sensitivity.

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“…When in chill coma, insect nerves are electrically silent and there is a lack of muscle excitability, the latter resulting from a progressive decline in muscle equilibrium potential during cooling (Staszak and Mutchmor, 1973;Goller and Esch, 1990;Hosler et al, 2000). Following prolonged cold exposure, two forms of chilling injury have been described: direct (cold shock) and indirect.…”

Section: Introductionmentioning

confidence: 99%

The role of the gut in insect chilling injury: cold-induced disruption of osmoregulation in the fall field cricket,Gryllus pennsylvanicus

MacMillan

Sinclair

2011

Journal of Experimental Biology

147

175

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SUMMARYTo predict the effects of changing climates on insect distribution and abundance, a clear understanding of the mechanisms that underlie critical thermal limits is required. In insects, the loss of muscle function and onset of cold-induced injury has previously been correlated with a loss of muscle resting potential. To determine the cause of this loss of function, we measured the effects of cold exposure on ion and water homeostasis in muscle tissue, hemolymph and the alimentary canal of the fall field cricket, Gryllus pennsylvanicus, during an exposure to 0°C that caused chilling injury and death. Low temperature exposure had little effect on muscle osmotic balance but it dissipated muscle ion equilibrium potentials through interactions between the hemolymph and gut. Hemolymph volume declined by 84% during cold exposure whereas gut water content rose in a comparable manner. This rise in water content was driven by a failure to maintain osmotic equilibrium across the gut wall, which resulted in considerable migration of Na + , Ca 2+ and Mg 2+ into the alimentary canal during cold exposure. This 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.Supplementary material available online at

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Flight muscle resting potential and species-specific differences in chill-coma

Cited by 114 publications

References 21 publications

The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

The effects of carbon dioxide anesthesia and anoxia on rapid cold-hardening and chill coma recovery in Drosophila melanogaster

Cold-acclimation improves chill tolerance in the migratory locust through preservation of ion balance and membrane potential

The role of the gut in insect chilling injury: cold-induced disruption of osmoregulation in the fall field cricket,Gryllus pennsylvanicus

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