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寒冷和制动应激诱导大鼠疼痛反应性及脑内甲硫氨酸脑啡肽样免疫反应性的变化。

Cold and immobilization stress-induced changes in pain responsiveness and brain Met-enkephalin-like immunoreactivity in the rat.

作者信息

Kurumaji A, Takashima M, Shibuya H

出版信息

Peptides. 1987 Mar-Apr;8(2):355-9. doi: 10.1016/0196-9781(87)90111-2.

Abstract

Pain responsiveness and Met-enkephalin-like immunoreactivity (MLI) were studied in the rat after cold (25 degrees C) and immobilization stress for different lengths of time (30 min, 90 min and 180 min). The 30-min stress-induced analgesia (as measured by the tail-flick method), which was partially antagonized by pretreatment with naloxone (5 mg/kg, SC), and the magnitude of this analgesia was less than that of the 90-min stress or 180-min stress. The 30-min stress resulted in a significant decrease in MLI in the mesolimbic area, striatum, hypothalamus and thalamus. After the 90-min stress, MLI was found to be significantly decreased in the prefrontal cortex, amygdaloid nuclei and piriform cortex, thalamus and hippocampus, while the 180-min stress failed to induce a significant change in any brain area tested. As such a change in MLI content was thought to be related to an increase in the activity of the endogenous Met-enkephalin neuronal system, the activation of this system by the stress, especially in the hypothalamus and thalamus, seemed to be associated with analgesia.

摘要

在大鼠经受不同时长(30分钟、90分钟和180分钟)的寒冷(25摄氏度)和固定应激后,对其疼痛反应性和甲硫氨酸脑啡肽样免疫反应性(MLI)进行了研究。30分钟应激诱导的镇痛作用(通过甩尾法测量),可被纳洛酮(5毫克/千克,皮下注射)预处理部分拮抗,且该镇痛作用的强度小于90分钟应激或180分钟应激所诱导的镇痛作用。30分钟应激导致中脑边缘区、纹状体、下丘脑和丘脑的MLI显著降低。90分钟应激后,在前额叶皮质、杏仁核、梨状皮质、丘脑和海马中发现MLI显著降低,而180分钟应激未能在任何测试脑区诱导出显著变化。由于认为MLI含量的这种变化与内源性甲硫氨酸脑啡肽神经元系统活性增加有关,应激对该系统的激活,尤其是在下丘脑和丘脑中的激活,似乎与镇痛作用相关。

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