Studies of Actions Mechanisms in Different Frequencies of Electroacupaucture Analgesia on Central Monoaminergic and Opioid Receptors

• Main Authors: Ming-Chien Yu, 游明謙
• Other Authors: Jaung-Geng Lin
• Format: Others
• Language: zh-TW
• Published: 1995
• Online Access: http://ndltd.ncl.edu.tw/handle/81952666845658752214

碩士 === 中國醫藥學院 === 中國醫學研究所 === 83 === There are many studies on the mechanism of antinociception of electro-acupuncture (EAc) in the past decades. It has been proved that antinociception of EAc was related to the concentration of neuropeptides (enkephalin, endorphin) and monoamines (5HT, NE). In order to understand the relationship of EAc analgesia and monoaminergic neurons and opioid receptors, this study was accomplished by the formalin test in ICR mice. The evidences suggest that (1) Exogenous 5-HT and NE enhanced the analgesic effect of the different frequencies of EAc, especially at 100 Hz. (2) The antinociception of EAc at different frequencies stimulation (2, 10 and 100 Hz) were attenuated by PCPA, and were potentiated by 5-HTP. (3) Naloxone could reverse the EAc analgesia of 2 Hz and 10 Hz but not 100 Hz. However, naltrindole could everse the EAc analgesia of 10 Hz and 100 Hz but not 2 Hz. (4) Prazosin and clonidine could potentiate the antinociception of different frequencies of EAc whereas yohimbine could reverse 2 Hz and 10 Hz EAc analgesia and potentiate 100 Hz EAc analgesia. (5) Pindobind-5-HT1A and LY-278584 could reverse the three different frequencies of EAc analgesia and ketanserin potentiate 100 Hz EAc analgesia. From the above results, we suggest that the analgesic effect of EAc is related to serotonergic and noradrenergic neurons at different frequency stimulations. In serotonergic pathway, EAc analgesia may be mediated via 5-HT1A and 5-HT3 receptors. Besides, 5-HT2 may be involved in high frequency EAc analgesia. In nor- adrenergic pathway, bothα1 andα2 receptors were involved in EAc analgesia and may be play in the opposite function. Moreover, the EAc analgesia may be mediated viaμ-opioid receptor at low frequency stimulation andδ-opioid receptor at high frequency stimulation.