Tepper J M, Nakamura S, Young S J, Groves P M
Brain Res. 1984 Sep 10;309(2):317-33.
The neurophysiological correlates of autoinhibition at the terminals of nigrostriatal dopaminergic neurons were studied by measuring the changes in antidromic excitability of nigrostriatal neurons following local infusions of various catecholamine agonists and antagonists into the neostriatum. Infusions of apomorphine or amphetamine reduced terminal excitability whereas the dopamine antagonists, haloperidol, fluphenazine or sulpiride, led to increases in terminal excitability. Alterations in antidromic excitability were constrained to the terminal regions and were not observed when infusions and excitability testing were performed in the medial forebrain bundle. The alpha-2 agonist, clonidine, did not alter dopaminergic terminal excitability. Our results indicate that pharmacological manipulations which have been shown to reduce the amount of stimulation-induced transmitter release from dopaminergic terminals are associated with a dopamine autoreceptor-mediated hyperpolarization and/or alteration in ionic conductance of the terminal membranes. These results are discussed with respect to mechanisms of autoinhibition in the central nervous system.
通过测量向新纹状体局部注射各种儿茶酚胺激动剂和拮抗剂后黑质纹状体神经元逆向兴奋性的变化，研究了黑质纹状体多巴胺能神经元终末自身抑制的神经生理学相关性。注射阿扑吗啡或苯丙胺可降低终末兴奋性，而多巴胺拮抗剂氟哌啶醇、氟奋乃静或舒必利则导致终末兴奋性增加。逆向兴奋性的改变局限于终末区域，在内侧前脑束进行注射和兴奋性测试时未观察到这种改变。α-2激动剂可乐定不会改变多巴胺能终末兴奋性。我们的结果表明，已证明可减少多巴胺能终末刺激诱导的递质释放量的药理学操作与多巴胺自身受体介导的超极化和/或终末膜离子电导改变有关。就中枢神经系统自身抑制机制对这些结果进行了讨论。
