Juel C
Comp Biochem Physiol C Comp Pharmacol Toxicol. 1983;76(1):203-8. doi: 10.1016/0742-8413(83)90064-6.
The rate of transmitter mobilization in identified dopaminergic synapses was decreased by the dopamine antagonists pimozide, chlorpromazine, haloperidol, cis-flupenthixol, curare, clozapine and high concentrations of ergometrine. The depolarizing postsynaptic potential was inhibited by pimozide, chlorpromazine, haloperidol, cis-flupenthixol, curare, clozapine, (+)-butaclamol and high concentrations of ergometrine. The hyperpolarizing synaptic potential was inhibited by naloxone, methysergide, (+)-butaclamol, haloperidol, 6-hydroxydopamine and low concentrations of ergometrine, while pimozide, cis-flupenthixol, trans-flupenthixol, curare, clozapine, promethazine, chlorpromazine and (-)-butaclamol had no clear effect. The presynaptic receptors involved in modulation of the mobilization rate showed similarities with the dopamine receptors mediating depolarizations. The dopamine antagonists changed dynamics of synaptic transmission.
在已确定的多巴胺能突触中,多巴胺拮抗剂匹莫齐特、氯丙嗪、氟哌啶醇、顺式氟奋乃静、箭毒、氯氮平和高浓度麦角新碱可降低递质动员速率。匹莫齐特、氯丙嗪、氟哌啶醇、顺式氟奋乃静、箭毒、氯氮平、(+)-布他拉莫和高浓度麦角新碱可抑制去极化突触后电位。纳洛酮、甲基麦角新碱、(+)-布他拉莫、氟哌啶醇、6-羟基多巴胺和低浓度麦角新碱可抑制超极化突触电位,而匹莫齐特、顺式氟奋乃静、反式氟奋乃静、箭毒、氯氮平、异丙嗪、氯丙嗪和(-)-布他拉莫则无明显作用。参与调节动员速率的突触前受体与介导去极化的多巴胺受体具有相似性。多巴胺拮抗剂改变了突触传递的动力学。