Abstract

Heat shock (45°C), cold shock (−10°C), and indirect chilling injury (a prolonged exposure to 2°C) did not interfere with the continuation of pharate adult development in the flesh fly, Sarcophaga crassipalpis, but such flies failed to eclose properly when the exposure was of sufficient duration. In all three forms of injury, development following the temperature treatments was also retarded. Among flies that were less severely affected and still capable of emerging as adults, the circadian time of adult eclosion shifted from near dawn to near the middle of the photophase, thus suggesting that the neurally-based clock is among the systems most vulnerable to heat-shock and cold-shock injury. Tensiometric records of ptilinum expansion revealed important differences in the nature of the injury caused by the different temperature stresses. Heat-shocked flies and those subjected to indirect chilling injury displayed the two behavioral programs normally associated with adult eclosion, the program for obstacle removal (POR) and the program for forward movement (PFM), but such flies failed to eclose because the muscle contractions generated by these motor patterns were insufficient for successful eclosion. In contrast, cold-shocked flies retained the capacity for strong muscle contraction, but the centrally-generated POR and PFM programs were altered. As the duration of cold shock increased, both patterns became more erratic; the PFM program was then lost completely, and in the most severe cases of cold-shock injury, flies lost the capacity to generate both programs. This suggests that neuronal damage is the likely cause of injury inflicted by cold shock.

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