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大鼠延髓微刺激产生的纳洛酮可逆性镇痛作用。

Naloxone-reversible analgesia produced by microstimulation in the rat medulla.

作者信息

Zorman G, Hentall I D, Adams J E, Fields H L

出版信息

Brain Res. 1981 Aug 24;219(1):137-48. doi: 10.1016/0006-8993(81)90273-0.

Abstract

Using microstimulation of the rostral medulla in the barbiturate-anesthetized rat, a map was constructed of loci for inhibition of the tail-flick response to noxious heat. Low threshold sites (less than or equal to 10 microA) were found in both the nucleus raphe magnus and the nucleus reticularis paragigantocellularis. Chronaxie determinations indicate that analgesia was not produced by activation of large myelinated axons of passage. Systemic naloxone only antagonized the inhibition generated from stimulation at low threshold sites. Inhibition from higher threshold sites, for example from the nucleus reticularis gigantocellularis, was not naloxone reversible. Depending on the area stimulated, either an opioid-or a non-opioid-mediated inhibition results from microstimulation within the rat medulla.

摘要

在巴比妥麻醉的大鼠中,通过对延髓嘴端进行微刺激,构建了一张抑制对有害热刺激甩尾反应的位点图谱。在中缝大核和巨细胞旁网状核中均发现了低阈值位点(小于或等于10微安)。时值测定表明,镇痛并非由传导的有髓大轴突的激活所产生。全身性纳洛酮仅拮抗低阈值位点刺激所产生的抑制作用。来自较高阈值位点(例如巨细胞网状核)的抑制作用,纳洛酮无法使其逆转。根据刺激的区域不同,大鼠延髓内的微刺激可产生阿片类或非阿片类介导的抑制作用。

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