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The effects of the alpha‐2 adrenoreceptor agonist clonidine on the activity of thermally classified neurons in anterior hypothalamus of the rat
Author(s) -
Perez Reinaldo,
Moore Andrew R.,
Griffin John D.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1053.25
Subject(s) - clonidine , agonist , hypothalamus , alpha (finance) , endocrinology , medicine , alpha 2 adrenergic receptor , thermoregulation , chemistry , anterior hypothalamus , receptor , construct validity , nursing , patient satisfaction
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 E 2 (PGE 2 ). 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.