This thesis investigates the hypothesis that thermoregulation may depend upon opposing responses of hot and cold temperature sensors with reciprocal inhibition between the efferent signals to the heat loss and heat production effectors, rather than upon comparison of a regulated variable with a temperature insensitive reference signal. A physical model was built to demonstrate that temperature regulation can work on this principle, and intracerebroventricular injections (ICV) of synaptically active substances were made into sheep to investigate the role of gamma-aminobutyric acid (GABA) as a neurotransmitter of reciprocal inhibition in thermoregulation. The model consisted of two inversely-related temperature-dependent signal generators connected to opposing correction effectors which served to heat and cool a plexiglass chamber. Reciprocal inhibition between the efferent pathways created a thermoregulatory null-zone which could be varied by manipulating signals converging onto either pathway to qualitatively simulate physiological responses to fever, hibernation and ICV injections of synaptically active substances. ICV injections of GABA or its agonist muscimol inhibited heat loss in the heat and heat production in the cold in sheep. An ICV injection of a GABA blocker prior to the ICV injection of an excitatory transmitter of either the heat production pathway in the heat or the heat loss pathway in the cold activated both heat production and heat loss effectors simultaneously. These results support the hypotheses that thermoregulation may depend upon opposing responses of sensor signals with reciprocal inhibition between the signals to opposing effectors and that GABA acts as the neurotransmitter of reciprocal inhibition.
Thesis (Ph.D.) University of Alaska Fairbanks, 1986
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