Vizi S E, Rónai A, Hársing L, Knoll J
Pol J Pharmacol Pharm. 1977 May-Jun;29(3):201-11.
It has been shown that dopamine inhibits the release of acetylcholine (ACh) from nerve terminals of caudate cholinergic interneurons, and the imbalance between dopaminergic and cholinergic system by 6-hydroxydopamine pretreatment leads to an increased ACh release. The Parkinson-syndrome induced by drugs which depress dopaminergic function either by reducing the output of dopamine, such as reserpine, or by antagonizing its action on DA receptors, as for instance haloperidol or chlorpromazine, can be attributed to the augmented release of ACh from caudate cholinergic nerve terminals and a consequent increase of cholinergic outflow from caudate nucleus. However, athetoid and choreiform hyperkinesis in patients and hypermotility in animals might result from increased dopaminergic outflow of nigro-striatal pathway and a consequent reduction in cholinergic neurosecretion of caudate nucleus.
已经表明，多巴胺抑制尾状核胆碱能中间神经元神经末梢乙酰胆碱（ACh）的释放，而6-羟基多巴胺预处理导致多巴胺能和胆碱能系统之间的失衡，从而使ACh释放增加。通过降低多巴胺输出（如利血平）或拮抗其对DA受体的作用（如氟哌啶醇或氯丙嗪）来抑制多巴胺能功能的药物所诱发的帕金森综合征，可归因于尾状核胆碱能神经末梢ACh释放增加以及尾状核胆碱能流出量随之增加。然而，患者的手足徐动和舞蹈样运动亢进以及动物的运动过度可能是黑质-纹状体通路多巴胺能流出增加以及尾状核胆碱能神经分泌随之减少所致。
