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Role of Serotonin 2A and 2C Receptors in Ketamine‐induced Hypothermia
Author(s) -
Murphy Tyler Joseph,
Murnane Kevin Sean
Publication year - 2016
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.30.1_supplement.930.5
Subject(s) - hypothermia , ketamine , thermoregulation , medicine , serotonin , agonist , receptor , 5 ht receptor , pharmacology , liraglutide , anesthesia , endocrinology , type 2 diabetes , diabetes mellitus
Anesthesia‐Induced Hypothermia (AIH) has been reported to cause many postoperative adverse effects. These effects include increased mortality, immunosuppression, increased risk of cardiac events, and a higher prevalence of surgical wound infections. Currently, there are few effective ways of preventing AIH besides pre‐warming fluids and gases for the patients during surgery, or relying on forced‐air heating systems. Although it is established that serotonin has a role in thermoregulation, the receptors responsible for such effects remain unclear. Here, we investigated the role of serotonin receptors in AIH using the 5‐HT 2A receptor antagonist M100907 and the 5‐HT 2C receptor agonist WAY‐163909. Core body temperature was determined through the use of a rectal probe and hypothermia was induced by ketamine in male, young adult Swiss‐Webster mice. We found that dose‐dependently and reliably ketamine induced hypothermia. Moreover, WAY‐163909 attenuated ketamine‐induced hypothermia. In contrast, ketamine‐induced hypothermia was exacerbated by M100907. These findings suggest a new clinical use for 5‐HT 2C receptor agonists, specifically to maintain body temperature during surgery. We will build upon these studies by conducting mechanistic pharmacological and neurobiological experiments, including immunohistochemical assays to determine the effects of these drugs on activity in the preoptic area of the anterior hypothalamus, the thermoregulatory center of the brain. Support or Funding Information This work was supported by institution funds supplied by the Mercer University College of Pharmacy, an honors thesis award supplied by Oglethorpe University, and a Summer Undergraduate Research Fellowship supplied by the American Society for Pharmacology and Experimental Therapeutics.