BODY CONSTRAINT AND DEVELOPMENTAL ARREST INGALLERIA MELLONELLAL.: FURTHER STUDIES

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Abstract
The sequence of events in insect development that follows activation of the prothoracic glands aumd culminates in molting or metamorphosis is now weil established but the mechanism by which the sequence is initiated at the appropriate time and place remains little understood. It is reasonable to suppose that several or nmany requirenments, such as nutritional state, location, and appropriate body form should be nmet before a larva molts, or enters time developmental crisis of pupation. If integrated infornmation about these factors converges upon neurosecretory cells, either to activate them, or release them from inhibition, it should be possible to delay release of neuroscretory material, and thus suspend development. Until the neural pathways to the neurosecretory cells of the brain are worked out, evidence of the mechanism of release can only be circumstantial : it must be shown in each case that a manipulation which suspends development is not acting at a point in the sequence beyond prothoracotropic hormone release. The capacity of implanted endocrine organs, or injected hormone to override developmental arrest provides suggestive, but not conclusive information about mechanisms of arrest. Treatments which nmay be expected to alter sensory input to the brain of Galleria nielionella, such as severing the ventral nerve cord or bodily constraint, prevent initiation of the barvab-pupal molting cycle and it has been suggested that these operations may inhibit time release of prothoracotropic hormone as a result of nmodifled proprioreceptive input (Edwards, 1967). Such treatments might in fact intervene in the molt controlling mechanisms at several levels: (a) by inhibiting the secretion of prothoracotropic hormone from the brain, (b) by blocking the response of the prothoracic glands to the hormone, or otherwise preventing the secretion of molting hormone, or (c) by directly affectiumgthe capacity of epidermis to respond to timehormones. The aim of this study was to limit these possibilities. It is shown timat restraint neitlmer blocks timecapacity of the prothoracic glands to secrete ecdysone, nor the capacity of time epidermis to respond to ecdysone. The mechanism is thus limited to inhibition of brain activity. The precise means by which prothoracotropic hor mone is withheld reummains to be demonstrated, but the results are consistent with the hypothesis that nmodification of sensory input underlies the immhibition,and that least in the wax moth, body form is a significant factor.

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