Vidal Lucía, Durán Rafael, Faro Lilian R F, Alfonso Miguel
Department of Functional Biology and Health Sciences, University of Vigo, Vigo, Spain.
Toxicol Lett. 2008 May 30;178(3):181-4. doi: 10.1016/j.toxlet.2008.03.008. Epub 2008 Mar 21.
The possible role of acetylcholine receptors on the HgCl(2)-induced dopamine (DA) release from rat striatum was investigated by using in vivo brain microdialysis technique after administration of selective nicotinic and muscarinic receptor antagonists, mecamylamine and atropine, respectively. Intrastriatal infusion of 1mM HgCl(2) increased striatal DA to 1717.2+/-375.4% respect to basal levels. Infusion of 1mM HgCl(2) in 1mM mecamylamine pretreated animals produced an increase on striatal DA levels 58% less than that induced in non-pretreated animals. In the case of atropine, this treatment reduced 62% the effect produced by HgCl(2) as compared to non-pretreated rats. These data show that acetylcholine receptors could participate on HgCl(2)-induced dopamine release since administration of nicotinic and muscarinic receptor antagonists reduces HgCl(2) effects on DA release.
分别给予选择性烟碱样和毒蕈碱样受体拮抗剂美加明和阿托品后，采用体内脑微透析技术研究了乙酰胆碱受体在氯化汞诱导大鼠纹状体多巴胺（DA）释放中的可能作用。纹状体内注入1mM氯化汞使纹状体多巴胺水平相对于基础水平增加至1717.2±375.4%。在预先用1mM美加明处理的动物中注入1mM氯化汞，使纹状体多巴胺水平的增加比未预处理动物中诱导的增加少58%。就阿托品而言，与未预处理的大鼠相比，这种处理使氯化汞产生的效应降低了62%。这些数据表明，乙酰胆碱受体可能参与了氯化汞诱导的多巴胺释放，因为给予烟碱样和毒蕈碱样受体拮抗剂会降低氯化汞对多巴胺释放的影响。
