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Raffaello Papeschi, MD, MSc
Servizio di Psichiatria Ospedale Civile 55100 Lucca Italy

Arch Gen Psychiatry. 1988;45(5):501-502.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor.—

Charney et al,¹ in the December 1986 issue of the ARCHIVES, report the lack of efficacy of combined treatment with desipramine hydrochloride—yohimbine hydrochloride in refractory depression and conclude that this is evidence against the role of brain β-adrenergic receptor function in depression. The latter has been reported as reduced by the combination of these two drugs.²

However, the interpretation by Charney et al is not, in my view, so simple and straightforward. Besides the 2-adrenergic blockade and the effect on β-adrenergic receptor function, yohimbine possesses many other actions that might have obscured an antidepressant effect. Yohimbine inhibits tryptophan,³ may stimulate serotonin receptors,⁴ and, above all, may induce a preferential destruction of newly synthesized dopamine and a depletion of stored noradrenaline.⁵ Thus, when using such a complex pharmacologic tool as yohimbine, it is not possible to draw any direct clinical inference by ascribing it to only . . . [Full Text PDF of this Article]

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