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Robert H. Howland, MD
Western Psychiatric Institute and Clinic 3811 O'Hara St Pittsburgh, PA 15213

Arch Gen Psychiatry. 1995;52(2):156.

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

In their report on the use of pindolol to augment selective serotonin (5-HT) reuptake inhibitors and monoamine oxidase inhibitors, Artigas et al¹ suggest that this may be mediated by presynaptic 5-HTIA antagonism, resulting in enhanced serotonergic function. Buspirone, a 5-HT_IA agonist, also may be effective in augmenting selective 5-HT reuptake inhibitors in refractory depression.^2-5 Because pindolol and buspirone have opposite effects on 5-HT_IA function, their efficacy is therefore difficult to reconcile on this basis. Furthermore, it is not clear how 5-HT_IA antagonism could account for the effect of pindolol, because reduced sensitivity of presynaptic 5-HT_IA receptors is found in major depression.^6,7

A major metabolite of buspirone is the ₂-adrenergicantagonist 1-(2-pyrimidinyl)-piperazine.^8,9₂-Adrenergic antagonism by 1-(2-pyrimidinyl)-piperazine could enhance the release of norepinephrine and result in mood elevation,¹⁰ which is consistent with the mechanism of antidepressants such as mianserin¹¹ . . . [Full Text PDF of this Article]

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