The resting potential of cockroach muscle membrane

et al. 2016

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.

Section: Cold Acclimation Improves Ion Homeostasis During Cold Stressmentioning

confidence: 68%

Section: Cold Acclimation Improves Ion Homeostasis During Cold Stressmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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

Andersen

Folkersen

et al. 2016

“…If the remaining 20 mV of depolarization is driven by a change in V d , it may thus result from a cold-induced increase in P Na , or decrease in P K , which would drive membrane potential toward the muscle equilibrium potential for Na + (E Na =+28 mV; Fig. 3C) (Wareham et al, 1974).…”

Section: Discussion Chilling Depolarizes Insect Muscle Fibresmentioning

confidence: 99%

Cold-induced depolarization of insect muscle: Differing roles of extracellular K+ during acute and chronic chilling

Findsen

Pedersen

et al. 2014

111

Insects enter chill coma, a reversible state of paralysis, at temperatures below their critical thermal minimum (CT min ), and the time required for an insect to recover after a cold exposure is termed chill coma recovery time (CCRT). The CT min and CCRT are both important metrics of insect cold tolerance that are used interchangeably, although chill coma recovery is not necessarily permitted by a direct reversal of the mechanism causing chill coma onset. Nevertheless, onset and recovery of coma have been attributed to loss of neuromuscular function due to depolarization of muscle fibre membrane potential (V m does depolarize muscle resting potential and slow CCRT following prolonged cold exposure. However, onset of chill coma at the CT min relates to an as-yet-unknown effect of temperature on neuromuscular function.

“…This reduction in volume, which is probably caused by water following Na + osmotically, has the end result that hemolymph [K + ] increases in the reduced hemolymph volume (Koštal et al, 2004;MacMillan and Sinclair, 2011b;MacMillan et al, 2015a,d). Membrane resting potential is highly dependent on the cellular [K + ] gradient (Hoyle, 1954;Wareham et al, 1974;Fitzgerald et al, 1996) and hemolymph hyperkalemia therefore causes cellular depolarization that leaves the neuromuscular system unexcitable and slows chill coma recovery time; ultimately, hyperkalemia may cause cold-induced injury and death (Boutilier, 2001;Koštal et al, 2004;Findsen et al, 2013;MacMillan et al, 2015c).…”

Section: Introductionmentioning

confidence: 99%

Hemolymph metabolites and osmolality are tightly linked to cold tolerance ofDrosophilaspecies: a comparative study

Olsson

Nyberg

et al. 2016

Drosophila, like most insects, are susceptible to low temperatures, and will succumb to temperatures above the freezing point of their hemolymph. For these insects, cold exposure causes a loss of extracellular ion and water homeostasis, leading to chill injury and eventually death. Chill-tolerant species are characterized by lower hemolymph [Na + ] than chill-susceptible species and this lowered hemolymph [Na + ] is suggested to improve ion and water homeostasis during cold exposure. It has therefore also been hypothesized that hemolymph Na + is replaced by other 'cryoprotective' osmolytes in cold-tolerant species. Here, we compared the hemolymph metabolite profiles of five drosophilid species with marked differences in chill tolerance. All species were examined under 'normal' thermal conditions (i.e. 20°C) and following cold exposure (4 h at 0°C). Under benign conditions, total hemolymph osmolality was similar among all species despite chill-tolerant species having lower hemolymph [Na + ]. Using NMR spectroscopy, we found that chilltolerant species instead have higher levels of sugars and free amino acids in their hemolymph, including classical 'cryoprotectants' such as trehalose and proline. In addition, we found that chill-tolerant species maintain a relatively stable hemolymph osmolality and metabolite profile when exposed to cold stress while sensitive species suffer from large increases in osmolality and massive changes in their metabolic profiles during a cold stress. We suggest that the larger contribution of classical cryoprotectants in chill-tolerant Drosophila plays a non-colligative role for cold tolerance that contributes to osmotic and ion homeostasis during cold exposure and, in addition, we discuss how these comparative differences may represent an evolutionary pathway toward more extreme cold tolerance of insects.