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机构地区:[1]西安交通大学医学院生理学与病理生理学系环境与疾病相关基因教育部重点实验室,陕西西安710061
出 处:《西安交通大学学报(医学版)》2006年第1期4-10,41,共8页Journal of Xi’an Jiaotong University(Medical Sciences)
基 金:国家自然科学基金资助项目(No.30270453)
摘 要:目的研究μ-和δ-阿片受体在介导丘脑中央下核(Sm)内阿片诱发的抗伤害感受效应中的作用。方法用自动检测系统记录大鼠爪底皮下注射福尔马林诱发的伤害性行为,观察Sm内微量注射吗啡和选择性μ-和δ-阿片受体拮抗剂对伤害性行为的效应。结果吗啡(31 mmol/L,0.5μL)明显抑制福尔马林诱发的伤害性行为,这种效应可被μ-阿片受体拮抗剂-βfunaltrexamine(-βFNA,0.4 mmol/L,0.5μL)和naloxonazine(0.8 mmol/L,0.5μL)阻断,部分地被δ-受体拮抗剂naltrindole(0.4 mmol/L,0.5μL)阻断。结论Sm内注射吗啡诱发的抗伤害感受效应主要由μ-阿片受体介导,部分地由δ-受体介导。Objective To investigate whether the μ- and δ- opioid receptors were involved in mediating the antinociceptive effect of opioid injection into the nucleus submedius (Sm). Methods Nociceptive behavior produced by subcutaneous injection of formalin (65 mmol/L, 50 μL) into the hind paw of the rat was assessed quantitatively using an automated movement detection system. The effects of morphine and selective μ- and δ- opioid receptor antagonists microinjected unilaterally into the Sm were determined in the awake rats. Results Morphine (31 mmol/L, 0. 5μL) depressed the nociceptive behavior elicited by formalin, and this effect was antagonized completely by the selective μ-receptor antagonist β-funaltrexamine (β-FNA, 0. 4 mmol/L, 0. 5 μL) and naloxonazine (0.8 mmol/L, 0.5μL), and partly by the δ-receptor antagonist naltrindole (0.4 mmol/L, 0.5μL). Administration of morphine into thalamic regions more than 0. 5 mm dorsal to the Sm had no effect on the nociceptive behavior. Conclusion Antinociceptive effects produced by opioid acting on Sm neurons are mediated mainly by μ-opioid receptors, and partly by δ-receptors.
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