Abstract
In response to infection, noradrenergic vagal afferents to the hypothalamus may be responsible for a rapid biphasic shift in thermoregulatory control. An initial hypothermic shift may result from the activation of alpha-2 adrenoreceptors, which is followed by an enduring hyperthermic response that is initiated by activation of alpha-1 andrenoreceptors and prolonged by the presence of prostaglandin E2 (PGE2). While previous studies from our lab have characterized the effects of PGE2 (Ranels & Griffin, 2003) and the alpha-1 agonist Cirazoline (Imbery et al., 2007), this study recorded the in vitro single-unit activity of thermally classified anterior hypothalamic neurons in response to the alpha-2 adrenoreceptor agonist Clonidine (100 μM). Based on their responses to temperature, warm sensitive neurons (m > 0.8 impulses.s-1.oC-1) showed significant increases in firing rate while temperature insensitive neurons showed significant decreases in firing rate. These changes would result in a hypothermic response according to Hammel's model, demonstrating the role of this adrenoreceptor subtype in temperature regulation. This research was supported by grants from the NIH (NS053794, NS065461 & NS053794-S1) and in part by a Howard Hughes Medical Institute grant through the Undergraduate Science Program to the College of William and Mary.
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