Saner A, Pletscher A
Eur J Pharmacol. 1977 Mar 21;42(2):155-60. doi: 10.1016/0014-2999(77)90355-7.
Apomorphine completely antagonized the reserpine-induced enhancement of the striatal 3,4-dihydroxyphenylalanine (dopa) accumulation seen after administration of the decarboxylase inhibitor 3-hydroxybenzylhydrazine (NSD 1015). Reserpine-like drugs, e.g. Ro 4-1284 and Ro 4-9040, markedly enhanced the striatal dopa accumulation (due to NSD 1015) in normal animals but not in rats treated with reserpine plus apomorphine. Haloperidol enhanced the striatal dopa accumulation to a similar extent in normal and in reserpine-apomorphine-treated animals. Chlorpromazine also caused an enhancement of striatal dopa accumulation in both types of animals, but its potency was somewhat higher in normal rats than in those treated with reserpine plus apomorphine. In conclusion, reserpinized animals treated with apomorphine appear to be useful models for differentiating whether a drug enhances striatal DA turnover by interference with granular DA storage or by blockade of DA receptors. The latter seems to be the main mechanism of action of neuroleptic drugs.
阿扑吗啡完全拮抗了利血平诱导的纹状体3,4-二羟基苯丙氨酸（多巴）蓄积增强，这种增强现象在给予脱羧酶抑制剂3-羟基苄基肼（NSD 1015）后出现。利血平样药物，如Ro 4-1284和Ro 4-9040，在正常动物中显著增强了（因NSD 1015所致的）纹状体多巴蓄积，但在给予利血平和阿扑吗啡的大鼠中则不然。氟哌啶醇在正常动物和经利血平-阿扑吗啡处理的动物中，使纹状体多巴蓄积增强至相似程度。氯丙嗪在这两种类型的动物中也都导致纹状体多巴蓄积增强，但其效力在正常大鼠中略高于经利血平加阿扑吗啡处理的大鼠。总之，用阿扑吗啡处理的利血平化动物似乎是区分一种药物是通过干扰颗粒状多巴胺储存还是通过阻断多巴胺受体来增强纹状体多巴胺周转的有用模型。后者似乎是抗精神病药物的主要作用机制。
