Neural Mechanisms of Thermoregulation in the Rabbit, Oryctolagus Cuniculus
Gordon, Christopher John
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Permalink
https://hdl.handle.net/2142/68304
Description
Title
Neural Mechanisms of Thermoregulation in the Rabbit, Oryctolagus Cuniculus
Author(s)
Gordon, Christopher John
Issue Date
1980
Department of Study
Physiology and Biophysics
Discipline
Physiology
Degree Granting Institution
University of Illinois at Urbana-Champaign
Degree Name
Ph.D.
Degree Level
Dissertation
Keyword(s)
Biology, Animal Physiology
Language
eng
Abstract
The preoptic/anterior hypothalamus (POAH) is considered a prime integrative site for thermoregulatory control in mammals. Certain neurotropic agents can alter the activity of the POAH and thus affect thermoregulatory control. The major objective of this study is to investigate the changes in POAH neural activity during neurotropic agent-induced alterations in thermoregulation.
Male, New Zealand white rabbits (Oryctolagus cuniculus) were implanted with cannulae to record neuron activity, heat or cool the POAH, and inject neurotropic agents into the lateral ventricle or directly into the POAH. To avoid the depressant effects of anesthetics on neuron activity single units were recorded in the unanesthetized state.
Ventricular or direct POAH injections of norepinephrine (NE) results in vasoconstriction and hyperthermia while 5-hydroxytryptamine (5-HT) injections promote vasodilation and hypothermia. Cold-sensitive neurons were consistently facilitated by NE and inhibited by 5-HT. On the other hand, ventricular injections of 5-HT facilitated the activity of warm-sensitive neurons. NE and 5-HT altered the thermal-sensitivity of some POAH neurons.
The release of prostaglandin (PG) E in the POAH is thought to be one of the final steps in febrogenesis. PGE(,2) consistently facilitated the firing rate of cold-sensitive neurons and ventricular, but not direct POAH injections, inhibited the firing rate of warm-sensitive neurons. Ventricular and direct POAH injections of PGE(,2) occasionally altered neuron thermal sensitivity.
Some POAH neurons exhibited "infraslow" oscillations in firing rate which were similar to the rhythmic fluctuations in ear temperature. The oscillations in firing rate could be initiated or prevented with thermal and/or neurochemical stimulation of the POAH.
A significant number of thermal sensitive neurons were facilitated or inhibited with a sudden acoustic stimulus. A 500 millisecond sound pulse affected the activity of some units for over 5.0 seconds.
Some POAH neurons were stimulated by heating the back skin with radiant heat. The opiate peptide, beta endorphin, converted warm-responsive neurons to cold-responsive while cold-responsive neurons were converted to warm- or thermal-unresponsive.
The spike trains were analyzed for changes in the distribution of interspike intervals (ISI's). NE, 5-HT, and PGE(,2) elicited specific changes in the ISI distribution during normeothermia and POAH cooling.
The data of changes in POAH neuron activity during thermal and/or neurotropic stimulation are used to construct a functional model for thermoregulatory control. Past models for temperature control are amended to account for the neurological findings of this study.
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