Abstract
This review examines recent findings about the endocrine basis of larval diapause. Evidence has accumulated to support the view that larval diapause is regulated.by distinctive endocrine interactions. While the lack of the molting hormone, ecdysone, causes the arrest of morphogenesis in both diapausing larvae and pupae, the mecha nism leading to the inactivity of the ecdysial glands appears to differ between these life stages. The recent discovery of a juvenile hormone (JH) involvement in the regulation of the larval diapause of two species (24, 144) indicates that at least some species of diapausing larvae retain activity within their endocrine system. This finding has underscored the need to further examine the extent of endocrine activity during larval diapause. For background information, several reviews are available on insect endocrinology (36, 44, 139) and on the physiology and ecology of diapause (35, 87, 121). Hormonal failure and JH regulation are the two principal theories which have been developed to explain larval diapause. The hormonal failure theory was devel oped originally to explain the endocrine basis of pupal diapause (136138), and proposes that diapause is instituted when the cerebral neurosecretory (NS) system becomes inactive and the corpora cardiaca stop releasing the ecdysiotropin that is required to stimulate the ecdysial glands to secrete ecdysone. Morphogenesis resumes after the corpora cardiaca renew their release of ecdysiotropin. The dia pause state, therefore, is thought to be distinguished by complete inactivity in the endocrine system, including the corpora allata. This theory has been extended to explain the endocrine basis of larval diapause (56, 7 1, 135). Conversely, the JH regulation theory proposes that diapausing larvae, unlike diapausing pupae, retain actively secreting corpora allata and that JH initiates and maintains diapause by regulating the secretion of ecdysiotropin (24, 144). The corpora allata are thought to be controlled by ordinary and NS neurones from the brain. An intermediate titer of JH associated with diapause is believed to arrest morphogenesis by inhibiting
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