The α 2A-adrenoceptor subtype is not involved in inflammatory hyperalgesia or morphine-induced antinociception

Abstract

The purpose of the present study was to investigate the role of the α 2A-adrenoceptor subtype in inflammatory hyperalgesia, and in adrenergic–μ-opioid interactions in acute pain and inflammatory hyperalgesia. Behavioral responses to mechanical and thermal stimuli were studied in α 2A-adrenoceptor knockout mice and their wild-type controls. Thermal nociception was evaluated as paw withdrawal latencies to radiant heat applied to the hindpaws. Mechanical nociception was measured using von Frey monofilament applications to the hindpaws. Mechanical and thermal hyperalgesia, induced with intraplantar carrageenan (1 mg/40 μl) were compared in α 2A-adrenoceptor knockout and wild-type mice. The effects of the systemically administered μ-opioid receptor agonist morphine (1–10 mg/kg) were evaluated on mechanical withdrawal responses under normal and inflammatory conditions in knockout and wild-type mice. Withdrawal responses to radiant heat and von Frey monofilaments were similar in α 2A-adrenoceptor knockout and wild-type mice before and after the carrageenan-induced hindpaw inflammation. Also, the antinociceptive effects of morphine in mechanical nociceptive tests were similar before and after carrageenan-induced hindpaw inflammation. Our observations indicate that α 2A-adrenoceptors are not tonically involved in the modulation of inflammation-induced mechanical and thermal hyperalgesia. In addition, α 2A-adrenoceptors do not appear to play an important role in μ-opioid receptor-mediated antinociception or antihyperalgesia.