A role for the cytoskeleton in heat-shock-mediated thermoprotection of locust neuromuscular junctions.

A prior hyperthermic stress (heat shock) can induce thermoprotection of neuromuscular transmission in Locusta migratoria extensor tibiae muscle measured 4 h after the onset of the heat shock. It is not clear what effect an acute hyperthermic stress may have on the nervous system's ability to tolerate thermal stress, that is, before increased expression of heat-shock proteins. We found that over consecutive thermal stress tests, failure temperature was not altered in either heat-shock or control animals. This suggests that protective mechanisms are not established in the short term (within one hour). Various members of the heat-shock protein family interact with elements of the cytoskeleton. We found that preexposure of the preparation to cytoskeletal stabilizing drugs induced thermoprotection, while preexposure to cytoskeletal disrupting drugs disrupted the ability to confer and maintain thermoprotection. We conclude that thermoprotection relies on a stable cytoskeleton and suggest that members of the heat shock protein family are involved.