Prikhozhan A V, Kovalev G I, Raevskiĭ K S
Biull Eksp Biol Med. 1990 Dec;110(12):624-6.
Amitriptyline, imipramine, desipramine, viloxazine, moclobemide and its derivative, novel antidepressant befol (10(-6)-5 x 10(-4) M) decreased by 12-20% K(+)-stimulated 3H-D-asp release from perfused synaptosomes of rat brain cortex. Glutamic acid diethyl ester (GDEE) (10(-4) M) antagonized the effect of amitriptyline, imipramine, desipramine and befol and reversed the effect of moclobemide and viloxazine. Among neuroleptics studied, only carbidine, which possesses antidepressant activity together with antipsychotic one in clinics, decreased 3H-D-asp release by GDEE-sensitive mechanism. Effect of haloperidol and chlorpromazine was not affected by GDEE. It is concluded that autoregulatory mechanism on the terminals of glutamatergic neurons may be involved in the antidepressant action.
阿米替林、丙咪嗪、地昔帕明、维洛沙嗪、吗氯贝胺及其衍生物新型抗抑郁药befol（10⁻⁶ - 5×10⁻⁴ M）可使大鼠大脑皮层灌流突触体中K⁺刺激的³H-D-天冬氨酸释放减少12 - 20%。谷氨酸二乙酯（GDEE）（10⁻⁴ M）拮抗阿米替林、丙咪嗪、地昔帕明和befol的作用，并逆转吗氯贝胺和维洛沙嗪的作用。在所研究的抗精神病药物中，只有在临床上兼具抗抑郁活性和抗精神病活性的卡比定，通过GDEE敏感机制降低³H-D-天冬氨酸释放。氟哌啶醇和氯丙嗪的作用不受GDEE影响。结论是谷氨酸能神经元终末的自动调节机制可能参与了抗抑郁作用。
