Romero L, Hervás I, Artigas F
Department of Neurochemistry, Instituto de Investigaciones Biomédicas de Barcelona, CSIC, Spain.
Neurosci Lett. 1996 Nov 22;219(2):123-6. doi: 10.1016/s0304-3940(96)13199-2.
The increases in extracellular serotonin (5-hydroxytryptamine; 5-HT) produced by some antidepressent drugs in forebrain are attenuated by the activation of somatodendritic 5-HT1A autoreceptors by the excess 5-HT induced by these agents in the midbrain raphe. Using microdialysis, we have examined the effects of the selective 5-HT1A antagonist WAY-100635 in rats pretreated with the selective 5-HT reuptake inhibitors (SSRIs) citalopram, fluoxetine, fluvoxamine, the tricyclic antidepressants clomipramine and desipramine and the monoamine oxidase inhibitor phenelzine. WAY-100635 markedly potentiated the increases in 5-HT produced by the SSRIs, clomipramine and phenelzine but it did not alter that produced by desipramine. These results indicate that the effects of serotonergic antidepressant drugs (but not those of desipramine, which mainly blocks noradrenaline reuptake) can be potentiated by 5-HT1A autoreceptor blockade.
一些抗抑郁药物在前脑引起的细胞外5-羟色胺（5-羟色胺；5-HT）增加，会被这些药物在中脑缝核诱导产生的过量5-HT激活树突体5-HT1A自身受体所减弱。我们使用微透析技术，研究了选择性5-HT1A拮抗剂WAY-100635对预先用选择性5-羟色胺再摄取抑制剂（SSRIs）西酞普兰、氟西汀、氟伏沙明、三环类抗抑郁药氯米帕明和地昔帕明以及单胺氧化酶抑制剂苯乙肼预处理的大鼠的影响。WAY-100635显著增强了SSRIs、氯米帕明和苯乙肼引起的5-HT增加，但并未改变地昔帕明引起的5-HT增加。这些结果表明，5-HT1A自身受体阻断可增强血清素能抗抑郁药物（但不包括主要阻断去甲肾上腺素再摄取的地昔帕明）的作用。
