The 5-HT1A antagonist WAY-100635 selectively potentiates the presynaptic effects of serotonergic antidepressants in rat brain

被引：105

作者：

Romero, L ^{[1
]}

Hervas, I ^{[1
]}

Artigas, F ^{[1
]}

机构：

[1] CSIC,INST INVEST BIOMED,DEPT NEUROCHEM,ES-08034 BARCELONA,SPAIN

来源：

NEUROSCIENCE LETTERS | 1996年 / 219卷 / 02期

关键词：

5-hydroxytryptamine(1A) receptor antagonists; 5-hydroxytryptamine uptake inhibitors; citalopram; clomipramine; desipramine; fluoxetine; fluvoxamine; phenelzine;

D O I：

10.1016/S0304-3940(96)13199-2

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The increases in extracellular serotonin (5-hydroxytryptamine; 5-HT) produced by some antidepressant 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.

引用

页码：123 / 126

页数：4

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