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Chawki Benkelfat, MD; Bernard Seletti, MD; Roberta M. Palmour, PhD; Jean Hillel, MD; Mark Ellenbogen; Simon N. Young, PhD
Department of Psychiatry McGill University 1033 Pine Ave W Montreal, Quebec, Canada H3A 1A1

Arch Gen Psychiatry. 1995;52(2):154-155.

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

Delgado et al¹ have reported that acute tryptophan depletion reversed antidepressantinduced remission in patients with major depression; the reappearance of depressive symptoms was more often observed in depressed patients treated with serotonergic antidepressants. In their study, five of the 21 patients investigated were treated with a combination of antidepressant (desipramine hydrochloride, fluvoxamine) and lithium carbonate. We adopted a similar paradigm to investigate the extent to which the same effect would be seen in patients with affective disorder who were treated with lithium only. Clinically, lithium displays a unique pharmacological profile: weak intrinsic antidepressant properties, useful as an augmenting agent to potentiate the effectiveness of other antidepressants, antimanic, and mood stabilizer. The molecular effects mediating these various pharmacological properties are complex and almost certainly involve multiple neurotransmitters, transduction mechanisms, and/or second messenger systems. One current theory is that lithium exerts some of its therapeutic effects, ie, potentiation of antidepressant treatments . . . [Full Text PDF of this Article]

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