Journal
BRAIN RESEARCH
Volume 1193, Issue -, Pages 93-101Publisher
ELSEVIER
DOI: 10.1016/j.brainres.2007.12.016
Keywords
hypothalamus; thermoregulation; hyperthermia; norepinephrine; Cirazoline
Categories
Funding
- Howard Hughes Medical Institute Funding Source: Medline
- NINDS NIH HHS [R15 NS053794-01, NS053794, R15 NS053794] Funding Source: Medline
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Peripheral exposure to LPS induces a biphasic fever thought to be initiated via vagal afferents to the preoptic area of the anterior hypothalamus (POAH), an important thermoregulatory control center in the brain. Previous studies have shown that norepinephrine synaptically mediates this Prostaglandin E-2 (PGE(2)) -dependent change in temperature through the selective activation of alpha-2 adrenoreceptors (AR). However, there is clear evidence that alpha-1 AR activation of thermoregulatory hypothalamic neurons will result in a rapid hyperthermia that is not dependent on PGE(2). This direct action of norepinephrine in the POAH was tested in the present study by recording the single-unit activity of POAH neurons. in a tissue slice preparation from the adult male rat, in response to temperature and the selective alpha-1 AR agonist Cirazoline (1-100 mu M). Neurons were classified as either warm sensitive or temperature insensitive. Warm sensitive neurons responded to Cirazoline with a decrease in firing rate, while temperature insensitive neurons showed a firing rate increase. These responses are similar to those reported for PGE(2) and suggest that both warm sensitive and temperature insensitive neurons in the POAH are important in mediating this alpha-1 AR-dependent hyperthermic shift in body temperature. Published by Elsevier B.V.
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