Date Thesis Awarded


Access Type

Honors Thesis -- Access Restricted On-Campus Only

Degree Name

Bachelors of Science (BS)




John D. Griffin

Committee Members

Paul D. Heideman

Ashley Haines

Carey Bagdassarian


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.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial-No Derivative Works 3.0 License.


Thesis is part of Honors ETD pilot project, 2008-2013. Migrated from Dspace in 2016.

On-Campus Access Only