Date Thesis Awarded

5-2010

Access Type

Honors Thesis -- Access Restricted On-Campus Only

Degree Name

Bachelors of Science (BS)

Department

Neuroscience

Advisor

John D. Griffin

Committee Members

Randolph A. Coleman

Matthew J. Wawersik

Abstract

Previous studies of the mechanisms of fever genesis have suggested that the prostanoid prostaglandin E2 (PGE2) plays a key role. PGE2 has been correlated with changing the firing rates of thermosensitive neurons within the preoptic and anterior regions of the hypothalamus (POAH), increasing the firing rates of temperature insensitive neurons while inhibiting warm sensitive neurons. PGE2 has four receptor subtypes, two of which (EP3 and EP4) have been implicated by most studies to be involved in febrogenesis. EP3 and EP4 receptors work by respectively decreasing or increasing the intracellular cAMP concentrations, suggesting an important role for cAMP dependent kinases in PGE2's modulation of the firing rate of thermosensitive neurons. We hypothesized that the activation of these cAMP dependent kinases would increase the firing rates of thermosensitive neurons. To test this hypothesis, single-unit recordings were made in a hypothalamic tissue preparation of neurons located in the POAH. The neurons recorded were classified as temperature insensitive or warm sensitive and then treated with 1μM sp-cAMP, an activator of cAMP dependent kinases. The majority of temperature insensitive neurons responded with a decrease in firing rate, which poses some interesting questions regarding the distribution and role of PGE2 receptors in the fever generation process.

Creative Commons License

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

Comments

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

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