A collection of 63 of the author's papers reprinted from journals / 1v. (various paging) : / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (D.Sc.)--University of Adelaide, Dept. of Physiology, 1977

Thesis (D.Sc.) -- University of Adelaide, Dept. of Physiology, 1977. / A collection of 63 of the author's papers reprinted from journals.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1983. / Typescript. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references (leaves 242-266).

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published_or_final_version / Molecular Biology / Master / Master of Philosophy

Environmental temperature is arguably one of the most important abiotic physical factors affecting insect behaviour. Temperature affects virtually all physiological processes including those that regulate nervous system function. It is therefore not surprising that animals have evolved adaptations that confer tolerance to heat stress and allow for continued behaviour as ambient temperature fluctuates. Most animals have central nervous system (CNS) responses to heat shock (HS) preconditioning which extend the thermal operating range of neural circuits during exposure to extreme heat. It is unclear how HS preconditioning confers CNS thermotolerance. I used the migratory locust (Locusta migratoria), an animal that inhabits environments that can have large fluctuations in ambient temperature daily, to examine how neuronal circuits cope with temperatures stress. Using the ventilatory central pattern generator (vCPG) as a model circuit I was able to address how the CNS switches on adaptations which provide protection against heat stress. vCPG thermotolerance was manifested as an increase in the thermal operating range and a decrease in the length of time required to recover vCPG activity when temperature stress was removed. I investigated the octopaminergic (OA/cAMP/PKA) and nitrergic (NO/cGMP/PKG) signalling pathways and tested their involvement in conferring thermotolerance to the vCPG during heat stress. I found that long applications of octopamine, or increased adenylate cyclase activity generated vCPG thermotolerance and was dependent upon transcription and translation. In addition I found that HS-treated locust had significantly reduced nitric oxide (NO) production during heat stress, and when I pharmacologically reduced PKG activity vCPG thermotolerance was generated. However, unlike octopamine treatment thermotolerance could be observed within minutes following PKG inhibition. Thus I conclude that the octopaminergic and nitrergic pathways coordinate long- and short-term protective modulation of the locust CNS. / Thesis (Ph.D, Biology) -- Queen's University, 2009-08-27 16:11:09.581