Anoxia induces thermotolerance in the locust flight system

SUMMARYHeat shock and anoxia are environmental stresses that are known to trigger similar cellular responses. In this study, we used the locust to examine stress cross-tolerance by investigating the consequences of a prior anoxic stress on the effects of a subsequent high-temperature stress. Anoxic stress and heat shock induced thermotolerance by increasing the ability of intact locusts to survive normally lethal temperatures. To determine whether induced thermotolerance observed in the intact animal was correlated with electrophysiological changes, we measured whole-cell K+ currents and action potentials from locust neurons. K+ currents recorded from thoracic neuron somata were reduced after anoxic stress and decreased with increases in temperature. Prior anoxic stress and heat shock increased the upper temperature limit for generation of an action potential during a subsequent heat stress. Although anoxia induced thermotolerance in the locust flight system, a prior heat shock did not protect locusts from a subsequent anoxic stress. To determine whether changes in bioenergetic status were implicated in whole-animal cross-tolerance, phosphagen levels and rates of mitochondrial respiration were assayed. Heat shock alone had no effect on bioenergetic status. Prior heat shock allowed rapid recovery after normally lethal heat stress but afforded no protection after a subsequent anoxic stress. Heat shock also afforded no protection against disruption of bioenergetic status after a subsequent exercise stress. These metabolite studies are consistent with the electrophysiological data that demonstrate that a prior exposure to anoxia can have protective effects against high-temperature stress but that heat shock does not induce tolerance to anoxia.

Insulin-like peptides are not involved in maturation or functional recovery of neural circuits in the locust flight system

We sought to manipulate maturation and functional recovery of locust flight circuitry by treating locusts with pharmacological doses of bovine anti-insulin and insulin. Anti-insulin treatment of maturing locusts caused reduced growth of the thoracic nervous system, lower body weight, and softer cuticles compared with control locusts. We were unable to block either maturation or recovery of flight circuitry with anti-insulin. We propose that insulin-related peptides are involved in growth and cuticular changes during adult maturation, but have no role in promoting neuronal sprouting during this period or as a result of injury.Key words: insulin, maturation, functional recovery, proprioceptors, flight.