Lemasson M H, Bonnet J J, Costentin J
Biochem Pharmacol. 1984 Jul 1;33(13):2137-41. doi: 10.1016/0006-2952(84)90584-7.
On striatal synaptosomal preparations, using a double labelling test, numerous antidepressant drugs demonstrated an inhibitory effect on [3H]DA uptake at the same high concentrations producing a [14C]DA release. This releasing effect was also shared by non-antidepressant agents and was observed on synaptosomes preloaded with [3H]5HT. The imipramine-induced release of DA was not modified by increasing concentration of K+, by decreasing concentration of Na+, by deleting Ca2+ from the incubation medium, or by blocking the catecholamine uptake systems with nomifensine or cocaine. The imipramine effect was reversible and was possibly initiated by a transient physico-chemical modification of the synaptosomal membrane. It was concluded that the DA uptake carrier is probably not involved in the effect of these drugs.
在纹状体突触体标本上,采用双标记试验,许多抗抑郁药物在产生[14C]多巴胺释放的相同高浓度下,对[3H]多巴胺摄取表现出抑制作用。这种释放效应也存在于非抗抑郁药中,并且在预先加载[3H]5-羟色胺的突触体上也能观察到。丙咪嗪诱导的多巴胺释放不受钾离子浓度增加、钠离子浓度降低、孵育培养基中钙离子去除,或用诺米芬辛或可卡因阻断儿茶酚胺摄取系统的影响。丙咪嗪的作用是可逆的,可能是由突触体膜的瞬时物理化学修饰引发的。得出的结论是,多巴胺摄取载体可能不参与这些药物的作用。