弓状核中阿片受体在细胞介素所致发热效应中的作用

本研究旨在了解弓状核内的阿片受体在体温调节中的作用。研究使用细胞介素ＩＬ１β做致热源。以自动推进器向ＳＤ雄性大鼠弓状核微量注射１μ１ＩＬ１β。在给药前３０ｍｉｎ分别向弓状核微量注射通常阿片受体拮抗剂纳洛酮（Ｎａｌ）、阿片受体μ、δ和κ各自特异性拮抗剂ＣＴＡＰ、ＮＴＩ和ｎｏｒＢＮＩ做预处理，用生理盐水（Ｓａｌ）做对照。结果表明：ＩＬ１β所致的升体温效应能被Ｎａｌ和ＣＴＡＰ阻断，提示弓状核中的阿片受体（主要是μ受体）参与或介导了ＩＬ１β的致热效应；δ和κ受体特异性拮抗剂阻断ＩＬ１β所致的体温升高效应不明显。提示δ和κ阿片受体参与体温调节的可能性较小。对照ＡＲＨ和ＰＯＡＨ中阿片受体在ＩＬ１β所致发热中的作用可发现：二者作用极为相似，这一结果有力地支持了弓状核是体温调节中枢重要组成部分的观点。

THE ROLE OF OPIOID RECEPTORS OF ARCUATE NUCLEUS IN CYTOKINE INDUCED HYPERTHERMIA

The present study is to define the role played by the opioid receptors of ARH in the regulation of body temperature. 1 microliter of IL-1 beta (as pyrogen) was injected into the ARH of male Sprague-Dawley rat with an automatic micromanipulator to induce hyperthermia. 30 minutes prior to the injection of pyrogen, the experimental groups were pre-treated with general opioid receptor antagonist naloxone (Nal), selective mu, delta, kappa receptor antagonists CTAP, NTI, nor-BNI respectively. Controls were pre-treated with saline. The results showed that IL-1 beta-induced hyperthermia was blocked by Nal and CTAP, suggesting the involvement of, or mediation by, ARH opioid receptors (mainly the mu type) in IL-1 beta-induced hyperthermia. The blockade by delta and kappa antagonists was not remarkable. Thus their participation in this process is less likely. The similarity between the roles of opioid receptors of ARH and POAH in IL-1 beta-induced hyperthermia strongly supports the view that ARH may be an important component of the thermoregulatory center.