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Abstract

Article Abstract

Serotonin (5-HT) selective reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors arethought to have a delayed onset of antidepressant action attributable in part to the decrease in firingactivity of 5-HT neurons they produce upon treatment initiation. As cell body 5-HT1A autoreceptorsdesensitize, 5-HT neuronal firing is restored. The agent pindolol, through its 5-HT1A receptor blockingproperty, has been shown to prevent the initial decrease in firing of rat 5-HT neurons associated withSSRI treatment. Four open-label studies put into evidence a significant acceleration of the antidepressanteffect of SSRIs when combined with pindolol. Four of five placebo-controlled studies have confirmedthis observation. Controlled trials indicate that a greater rate of response may be obtained bycombining pindolol from the beginning of the SSRI treatment. The strategy of adding pindolol to theregimen of SSRI-resistant patients also appears to produce a therapeutic effect in a significant proportionof patients.