Prolactin in patients with major depressive disorder and in healthy subjects. II. Longitudinal study of basal prolactin and post-TRH-stimulated prolactin levels.

Longitudinal investigations of basal prolactin (PRL) and prolactin concentrations following thyrotopin-releasing hormone (TRH) stimulation (delta PRL) were conducted in 17 patients with major depressive disorder and healthy subjects. The patients were being treated with either clomipramine or maprotiline. Both basal and delta PRL increased significantly after clinical response during treatment with both drugs. However, these increases in basal and delta PRL were independent of each other. Surprisingly, elevations of basal PRL were significantly greater in responders than in nonresponders, whereas those in delta PRL showed no corresponding significant difference. These results suggest that the two drugs stimulate basal and delta PRL by different mechanisms. The increases in basal prolactin levels found in responders may possibly be due to weaker inhibition of prolactin due to "down-regulated" beta adrenergic receptors and/or enhanced activity of supersensitive serotonergic receptors. Neither basal PRL nor delta PRL proved to be a predictor of therapy response. The intraindividual retest reliabilities of both basal and delta PRL in healthy subjects was so good that a single blood sample would seem to be sufficient for investigating most issues involving PRL in psychiatric patients.