期刊
EUROPEAN JOURNAL OF PHARMACOLOGY
卷 509, 期 1, 页码 37-42出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2004.12.015
关键词
dint (2 ',6 '-dimethyl-L-tyrosine); endomorphin; antinociception; spinal; supraspinal; antagonist
The potent opioid [Dmt(1)]endomorphin-2 (Dmt-Pro-Phe-Phe-NH2) differentiated between the opioid receptor subtypes responsible for the antinociception elicited by endomorphin-2 in mice. Antinociception, induced by the intracerebroventricular administration of [Dmt(1)]endomorphin-2 and inhibited by various opioid receptor antagonists [naloxone, naltrindole, beta-funaltrexamine, naloxonazine], was determined by the tail-flick (spinal effect) and hot-plate (supraspinal effect) tests. The opioid receptor subtypes involved in [Dmt(1)] endomorphin-2-induced antinociception differed between these in vivo model paradigms: naloxone (non-specific opioid receptor antagonist) and beta-funaltrexamine (irreversible mu(1)/mu(2)-opioid receptor antagonist) blocked antinociception in both tests, although stronger inhibition occurred in the hot-plate than the tail-flick test suggesting involvement of other opioid receptors. Consequently, we applied naloxonazine (mu(1)-opioid receptor antagonist) that significantly blocked the effect in the hot-plate test and naltrindole (delta-opioid receptor antagonist), which was only effective in the tail-flick test. The data indicated that [Dmt(1)]endomorphin-2-induced spinal antinociception was primarily mediated by both mu(2)- and delta-opioid receptors, while a supraspinal mechanism involved only mu(1)/mu(2)-subtypes. (C) 2004 Elsevier B.V. All rights reserved.
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