Gaĭnetdinov R R, Budygin E A, Kovalev G I, Kudrin V S, Raevskiĭ K S
Biull Eksp Biol Med. 1992 Jul;114(7):47-9.
Effects of haloperidol (10(-7)-alpha 10(-5) M), trifluoperazine, metoclopramide, tiapride, sulpiride, thioridazine, clozapine remoxipride, raclopride, cis- and trans-isomers of carbidine, SCH 23390 (all at the 10(-6) M) on the K(+)-stimulated (28 mM) dopamine (DA) release from isolated rat striatum were studied. Haloperidol at the concentration of 10(-7) and 10(-6) M failed to affect, while at 10(-5) M the drug decreased the stimulated striatal DA release. Trifluoperazine, metoclopramide and tiapride were shown not to modify this process. Sulpiride, thioridazine, clozapine, remoxipride, raclopride, isomers of carbidine were found to increase significantly the stimulated striatal DA release. SCH 23390 failed to affect K(+)-stimulated release of DA in the striatum and also did not change K(+)-stimulated release enhancement produced by raclopride. It is suggested that the mechanism underlying observed effects of the drugs may contribute to pharmacological profile of atypical neuroleptics.
研究了氟哌啶醇（10⁻⁷ - 10⁻⁵M）、三氟拉嗪、甲氧氯普胺、硫必利、舒必利、硫利达嗪、氯氮平、瑞莫必利、雷氯必利、卡比多巴的顺式和反式异构体、SCH 23390（均为10⁻⁶M）对从分离的大鼠纹状体中K⁺刺激（28 mM）的多巴胺（DA）释放的影响。10⁻⁷和10⁻⁶M浓度的氟哌啶醇未能产生影响，而在10⁻⁵M时该药物降低了刺激的纹状体DA释放。三氟拉嗪、甲氧氯普胺和硫必利未显示出改变此过程。舒必利、硫利达嗪、氯氮平、瑞莫必利、雷氯必利、卡比多巴异构体被发现显著增加了刺激的纹状体DA释放。SCH 23390未能影响纹状体中K⁺刺激的DA释放，也未改变雷氯必利产生的K⁺刺激释放增强作用。提示所观察到的药物作用机制可能有助于非典型抗精神病药物的药理学特征。
