N-花生四烯酸氨基乙醇对小鼠肝片去甲肾上腺素递质体外释放的影响

Effects of Anandamide on the Release of Norepinephrine Neurotransmitter in Mice Liver Slices in vitro

目的探讨N-花生四烯酸氨基乙醇(anandamide,AEA)对肝组织中去甲肾上腺素(norepinephrine,NE)的影响及可能的神经生物学机制。方法制备肝片,用高效液相色谱-电化学(HPLC-ECD)方法检测AEA在体外对肝片NE释放的影响。结果随着AEA浓度的增加,AEA对肝片NE含钙自发性释放的抑制率(与对照组比较)逐渐下降并显现剂量-效应关系;而对无钙自发性释放抑制率先降低后升高,最低为11.43%。对肝片NE含钙去极化释放的抑制率先升高后降低,最高为39.17%,当AEA浓度达到20μmol/L时,对肝片NE的作用表现为刺激而不是抑制;对无钙去极化释放抑制率先升高后降低,最高为85.29%。结论AEA对NE自发性和去极化释放过程均有干扰作用,且该作用与钙离子有一定关系。

Objective To investigate the effect of anandamide （AEA） on the release of norepinephrine （NE） and the possible neurobiological mechanism. Methods Liver slices were prepared, and the release of NE in liver slices in vitro was determined by high performance liquid chromatography-electrochemical detector （HPLC-ECD）. Results With the increase of exposure to AEA, spontaneous release inhibition ratio of NE in liver slices was decreased dose-dependently in the presence of calcium. In the absence of calcium, spontaneous release inhibition ratio was firstly decreased and then increased, and the minimum was 11.43%. In the presence of calcium, depolarized release inhibition ratio was increased firstly and then decreased, and the maximum was 39. 17%. When AEA concentration was 20 μmol/L, AEA stimulated the release of NE. In the absence of calcium, depolarized release inhibition ratio was increased firstly and then decreased, and the maximum was 85.29%. Conclusion AEA could interfere with spontaneous and depolarized release of NE transmitter, which was related to the existence of calcium to some extent.