Tanganelli S, Fuxe K, von Euler G, Eneroth P, Agnati L F, Ungerstedt U
Department of Histology and Neurobiology, Pharmacology, Karolinska Institutet, Stockholm, Sweden.
J Neural Transm Gen Sect. 1990;81(3):183-94. doi: 10.1007/BF01245041.
The effects of apomorphine (0.05 mg/kg, i.p.) and cholecystokinin-8 (sulphated; CCK-8) were analyzed on the levels of dopamine and its metabolites using intrastriatal microdialysis in the adrenalectomized rat with or without corticosterone replacement treatment (5 mg/kg, twice daily for 7 days, last dose given 2 h before killing). Adrenalectomy did not affect the basal release of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC) or homovanillic acid (HVA). However, the apomorphine-induced decrease in dopamine release was attenuated following adrenalectomy. Furthermore, there was an enhancement of the apomorphine-induced decrease in DOPAC levels without any modulation of the apomorphine-induced effects on HVA levels. In contrast, the CCK-8-induced increase in dopamine levels was potentiated following adrenalectomy. This potentiation was fully counteracted by replacement treatment with corticosterone. These results indicate that corticosterone may be involved in the regulation of dopamine release, perhaps through glucocorticoid receptors in nigral dopamine cells controlling inter alia the synthesis of G-proteins involved in the regulation of dopamine autoreceptors and CCK-8 receptors located on dopamine nerve terminals or of the receptor proteins themselves.
采用纹状体内微透析技术,分析阿扑吗啡(0.05毫克/千克,腹腔注射)和胆囊收缩素-8(硫酸化;CCK-8)对去肾上腺大鼠多巴胺及其代谢产物水平的影响,这些大鼠接受或未接受皮质酮替代治疗(5毫克/千克,每日两次,共7天,最后一剂在处死前2小时给予)。去肾上腺并不影响多巴胺、3,4-二羟基苯乙酸(DOPAC)或高香草酸(HVA)的基础释放。然而,去肾上腺后,阿扑吗啡诱导的多巴胺释放减少减弱。此外,阿扑吗啡诱导的DOPAC水平降低增强,而阿扑吗啡对HVA水平的诱导作用未受任何调节。相反,去肾上腺后,CCK-8诱导的多巴胺水平升高增强。这种增强作用被皮质酮替代治疗完全抵消。这些结果表明,皮质酮可能参与多巴胺释放的调节,可能是通过黑质多巴胺细胞中的糖皮质激素受体,特别是控制参与多巴胺自身受体调节的G蛋白以及位于多巴胺神经末梢的CCK-8受体或受体蛋白本身的合成。