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The sensitivity of insect nervous systems to anoxia can be modulated genetically and pharmacologically, but the cellular mechanisms responsible are poorly understood. We examined the effect of a heat shock pretreatment (HS) on the sensitivity of the locust (Locusta migratoria) nervous system to anoxia induced by water immersion. Prior HS made locusts more resistant to anoxia by increasing the time taken to enter a coma and by reducing the time taken to recover the ability to stand. Anoxic comas were accompanied by surges of extracellular potassium ions in the neuropile of the metathoracic ganglion, and HS reduced the time taken for clearance of excess extracellular potassium ions. This could not be attributed to a decrease in the activity of protein kinase G, which was increased by HS. In homogenates of the metathoracic ganglion, HS had only a mild effect on the activity of Na(+)-K(+)-ATPase. However, we demonstrated that HS caused a threefold increase in the immunofluorescent localization of the α-subunit of Na(+)-K(+)-ATPase in metathoracic neuronal plasma membranes relative to background labeling of the nucleus. We conclude that HS induced trafficking of Na(+)-K(+)-ATPase into neuronal plasma membranes and suggest that this was at least partially responsible for the increased resistance to anoxia and the increased rate of recovery of neural function after a disturbance of K(+) homeostasis.

Na+-K+-ATPase trafficking induced by heat shock pretreatment correlates with increased resistance to anoxia in locusts

Na⁺-K⁺-ATPase trafficking induced by heat shock pretreatment correlates with increased resistance to anoxia in locusts