摘要
在轻度麻醉大鼠,电刺激下丘脑弓状核(ARH)大大延长了辐射热甩尾潜伏期,脊髓蛛网膜下腔注射(ith)κ阿片受体阻断剂nor-BNI对大鼠基础痛阈及ARH刺激引起的镇痛效应无明显影响,ithδ阿片受体阻断剂ICI 174864和不可逆的“阿片受体阻断剂β-FNA对基础痛阈仍无影响,但剂量依赖性地减弱了ARH刺激镇痛。结果提示,脊髓内的δ和μ受体参与了ARH对脊髓伤害性反射的下行性抑制。
In the lightly pentobarbital-anesthe arcuate nucleus of the hypothalamus (ARH)tized rat, intrathecal injections of three types of opiate stimulation-produced analgesia. A profound inhibireceptor antagonists were undertaken in order to fi tion of noxious heat-induced tail-flick reflex wasgure out the putative type of opioids processing the invariably observed during the electrical stimulation of the ARM. Intrathecal injection of ICI 174864 (δ-receptor antagonist) at a dose of 1.0 nmol dramatically attenuated the ARH stimulation-produced antinociception without affecting basal pain threshold. Control saline injection in the same animal had no significant influence on both the basal pain threshold and the brain stimulation-produced analgesia. Among the doses of 0.125, 0.25 and 0.5 nmol, a considerable reduction of the ARH analgesia was revealed following the injection of 0.5 nmol. In a separate group of animals, the intrathecal applicationof μ-receptor antagonist β-FNA at a dose range from 1.25 to 10.0 nmol dose-dependently blocked ARH analgesia. In contrast with that mentioned above, the intrathecal administration of K-receptor antagonist nor-BNI at a dose up to 25 nmol failed to modify the descending inhibitory effect of the ARH on the spinal nociceptive reflex as well as the basal pain threshold. The results obtained above indicate that the spinal d and μ but not K-opiate receptors are involved in mediation of the ARH stimulation-produced analgesia.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1991年第2期81-84,共4页
Chinese Journal of Pharmacology and Toxicology
关键词
阿片肽
疼痛
止痛
弓状核
受体
pain
analgesia
arcuate nucleus
opioid peptides
tail-flick latency
ICI 174864
nor-binaltorphimine
β-funaltrexamine
