Svensson T H, Dahlöf C, Engberg G, Hallberg H
Acta Psychiatr Scand Suppl. 1981;290:67-78. doi: 10.1111/j.1600-0447.1981.tb00710.x.
Activation of postsynaptic noradrenergic alpha 1-receptors may be involved in the mediation of psychomotor activating effects of tricyclic antidepressant (TCA) drugs. On the other hand, the pronounced sedative properties of some TCA drugs seem to be correlated with their alpha 1-receptor blocking capacity. The presynaptic alpha 2-receptors probably mediate the feed back inhibition of central NE neurons seen after administration of TCA drugs, particularly the secondary amines. Yet other antidepressants such as mianserin are potent antagonists at central alpha 2-receptors, a phenomenon which can even cause activation of brain NE neurons and form a basis for their therapeutic action. beta-Receptor activation in the brain is also suggested to participate in the therapeutic effect of several drugs, e.g. mianserin and the putative antidepressant agent salbutamol, a beta 2- receptor agonist. A reduced central beta-receptor activation may, accordingly, contribute to depressive symptoms associated with treatment with beta-adrenoceptor blocking drugs, both by their action per se as well as by secondary effects on the monoamine systems, which we recently have demonstrated. Facilitation of brain 5-HT neurotransmission seems to be achieved with several TCA drugs not only via inhibition of reuptake but also through sensitization of postsynaptic 5-HT receptors, developing during repeated treatment. In contrast the "presynaptic" 5-HT receptors do not show increased sensitivity during chronic TCA drug treatment, thus allowing for an enhanced synaptic effect of 5-HT induced by TCA drugs.
突触后去甲肾上腺素能α1受体的激活可能参与三环类抗抑郁药（TCA）精神运动激活作用的介导。另一方面，一些TCA药物显著的镇静特性似乎与其α1受体阻断能力相关。突触前α2受体可能介导TCA药物（尤其是仲胺类药物）给药后所见的中枢去甲肾上腺素能（NE）神经元的反馈抑制。然而，其他抗抑郁药如米安色林是中枢α2受体的强效拮抗剂，这一现象甚至可导致脑NE神经元激活，并构成其治疗作用的基础。脑内β受体激活也被认为参与了几种药物的治疗作用，例如米安色林和假定的抗抑郁药沙丁胺醇（一种β2受体激动剂）。因此，中枢β受体激活降低可能导致与β肾上腺素能受体阻断药治疗相关的抑郁症状，这既源于其本身的作用，也源于对单胺系统的继发效应，我们最近已证实了这一点。几种TCA药物不仅通过抑制再摄取，还通过反复治疗过程中突触后5-HT受体的敏化来促进脑内5-HT神经传递。相反，在慢性TCA药物治疗期间，“突触前”5-HT受体并未表现出敏感性增加，因此TCA药物可增强5-HT的突触效应。
