Kehr W, Carlsson A, Lindqvist M
Naunyn Schmiedebergs Arch Pharmacol. 1977 Mar;297(2):111-7. doi: 10.1007/BF00499920.
Axotomy of the ascending monoaminergic fibers by means of a complete cerebral hemitransection stimulated the formation of dopa during 30 min after inhibition of the aromatic amino acid decarboxylase with 3-hydroxybenzylhydrazine HCl, 100 mg/kg i.p., in c. striatum and the dopamine-rich part of the limbic system. Apomorphine, 0.5 mg/kg i.p., antagonized the accumulation of dopa not only on the intact but also on the lesioned side. Haloperidol, 2 mg/kg i.p., stimulated dopa accumulation on the intact side but could not further stimulate the increase in dopa caused by transection. When both drugs were given together, the inhibitory effect of apomorphine was fully counteracted by haloperidol on both sides. In the predominantly noradrenaline-innervated occipito-temporal cortex dopa formation was slightly higher on the lesioned than on the intact side and was not markedly influenced by apomorphine. In the rest of the hemispheres the apomorphine-induced decrease in dopa formation was more pronounced on the intact than on the lesioned side and was fully antagonized by haloperidol. The dopamine concentration was slightly higher in the lesioned c. striatum as compared to the intact side irrespective of the drugs administered. In c. striatum and the limbic system haloperidol caused a decrease in dopamine on the intact side which was not antagonized by additional treatment with apomorphine. Hemitransection caused a decrease in noradrenaline especially in the hemisphere portion. Neither apomorphine nor haloperidol or both drugs in combination changed the latter effect. In general, the tyrosine concentration tended to be higher on the lesioned than on the intact side in all brain structures investigated. The data support the view that a local receptor-mediated feedback mechanism exists which is controlling dopamine synthesis even in the absence of impulse flow.
通过完全大脑半横断术切断上行单胺能纤维，在用100mg/kg盐酸3-羟基苄肼腹腔注射抑制芳香族氨基酸脱羧酶后30分钟内，刺激了尾状核和边缘系统富含多巴胺部分的多巴形成。0.5mg/kg腹腔注射的阿扑吗啡不仅抑制了完整侧而且抑制了损伤侧的多巴积累。2mg/kg腹腔注射的氟哌啶醇刺激了完整侧的多巴积累，但不能进一步刺激横断引起的多巴增加。当两种药物同时给药时，氟哌啶醇在两侧都完全抵消了阿扑吗啡的抑制作用。在主要由去甲肾上腺素支配的枕颞叶皮质，损伤侧的多巴形成略高于完整侧，且不受阿扑吗啡的明显影响。在其余半球，阿扑吗啡引起的多巴形成减少在完整侧比损伤侧更明显，并被氟哌啶醇完全拮抗。无论给予何种药物，损伤的尾状核中的多巴胺浓度与完整侧相比略高。在尾状核和边缘系统中，氟哌啶醇导致完整侧的多巴胺减少，额外给予阿扑吗啡不能拮抗这种减少。半横断术导致去甲肾上腺素减少，尤其是在半球部分。阿扑吗啡、氟哌啶醇或两种药物联合使用均未改变后一种效应。总体而言，在所研究的所有脑结构中，损伤侧的酪氨酸浓度往往高于完整侧。这些数据支持这样一种观点，即存在一种局部受体介导的反馈机制，即使在没有冲动流的情况下也能控制多巴胺的合成。
