Modulation by desensitized nicotinic receptors on metabolism of DA in striatum derived from the hemiparkinsonian model

作     者：Fu-rong HAN Hai WANG Fu-rong HAN;Hai WANG

作者机构：Department of PharmacyBeijing Tongren HospitalCapital Medicine University Cardiovascular Drug Research CenterAcademy of Military Medical Sciences Cardiovascular Drug Research CenterThadweik Academy of Medicine 

出 版 物：《中国应用生理学杂志》 (Chinese Journal of Applied Physiology)

年 卷 期：2016年第32卷第6期

页      面：487-493页

核心收录：

学科分类：0710[理学-生物学] 1002[医学-临床医学] 07[理学] 071006[理学-神经生物学] 

基　　金：supported by a grant from the National Natural Science Foundations of China(30371641) 

主　　题：烟碱受体 帕金森病 代谢产物 纹状体 DA 多巴胺D2受体 模型 逆转录聚合酶链反应 

摘      要：Objective: The purpose of this study was to investigate the effects of desensitized nicotinic receptors(n ACh Rs) on striatal dopaminergic system in the hemiparkinsonian rats treated with 6-hydroxydopamine(6-OHDA). Methods: We examined the effects of desensitized n ACh Rs on the levels of dopamine(DA) and its metabolites, m RNA expression of dopamine receptor D1,D2 and monoamine oxidase B(MAO-B) in the striatum of 6-OHDA-lesioned rats using high-performance liquid chromatography and reverse transcription-polymerase chain reaction. Results: The results showed that n ACh Rs desensitization following repeated nicotine stimulation could reverse significantly the decrease of striatal DA and its metabolites levels and the increase in DA turnover in lesioned side striatum of hemiparkinsonian rats. Dopamine D1 receptor m RNA expression increased significantly, whereas dopamine D2 receptor m RNA expression remained unchanged in lesioned side striatum of nicotine-treated rats compared to 6-OHDA-lesioned rats when n ACh Rs were desensitized. Meanwhile, nicotine-treated rats displayed a significant decrease in MAO-B m RNA expression in lesioned side striatum compared to 6-OHDA-lesioned rats after n ACh Rs desensitization. Conclusion: These results suggest that n ACh Rs desensitization could promote DA level, upregulate dopamine D1 receptor expression and downregulate MAO-B expression in striatum of hemiparkinsonian rats.