Date Thesis Awarded
Bachelors of Science (BS)
John D. Griffin
Paul D. Heideman
Previous studies have proved that during a lipopolysaccharide (LPS) challenge, norepinephrine (NE) levels in the preoptic area of the mammalian hypothalamus (PO/AH) rise and are correlated with an increase in core body temperature. Whole animal studies have revealed that selective activation of the α1- and α2-adrenergic receptors (ARs) can, respectively, induce a hyperthermic or hypothermic thermoregulatory response. Therefore, we hypothesize that in accordance with established models of neural thermoregulation, firing rate responses to the α1-AR agonist Cirazoline and the α2-AR agonist Clonidine should differ with respect to thermosensitivity of the neuron. To characterize these responses, single-unit recordings of neurons in rat hypothalamic tissue preparation were made. Neurons were classified as either warm sensitive or temperature insensitive through manipulations in local temperature. This was followed by treatment of the neuron with either Cirazoline or Clonidine. As hypothesized, the majority of insensitive neurons increased their firing rate when exposed to Cirazoline and decreased their activity when introduced to Clonidine. When warm sensitive neurons were treated with Cirazoline, all responded with a decrease in activity, while most increased their firing rate during treatment with Clonidine. These AR responses, in accordance with current neural thermoregulatory models, would produce the same hypothermic or hyperthermic effects on core body temperature as seen with in vivo studies.
Speidell, Andrew, "The Effects of Cirazoline and Clonidine on the Firing Rates of Thermally Classified Neurons in the Anterior Hypothalamus of the Rat" (2008). Undergraduate Honors Theses. Paper 814.
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