Abstract
α 2-Adrenoceptor agonists potentiate opioid analgesia and alleviate opioid withdrawal. The effects of two α 2-adrenoceptor agonists, clonidine (2 mg/kg) and dexmedetomidine (20 and 100 μg/kg), and the α 1-adrenoceptor antagonist prazosin (0.5 mg/kg) were tested on morphine analgesia, tolerance, and withdrawal in wild-type and α 2A-adrenoceptor knock-out (KO) mice. Analgesia and tolerance were assessed with the tail-flick test. Withdrawal was precipitated with naloxone. Prazosin potentiated morphine analgesia equally in both genotypes. Clonidine and dexmedetomidine had no analgesic effects in α 2A-adrenoceptor KO mice, but morphine analgesia and tolerance were similar in both genotypes. α 2A-Adrenoceptor KO mice exhibited 70% fewer naloxone-precipitated jumps than wild-type mice; weight loss was similar in both genotypes. The α 2-adrenoceptor agonists reduced opioid withdrawal signs only in wild-type mice. We conclude that α 2A-adrenoceptors are not directly involved in morphine analgesia and tolerance, and not critical for potentiation of morphine analgesia by prazosin, but that α 2A-adrenoceptors modulate the expression of opioid withdrawal signs in mice.
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