Specific effects of escitalopram on neuroendocrine response

Abstract

Citalopram, a selective serotonin reuptake inhibitor, is used as a neuroendocrine probe in human subjects to assess serotonin function as reflected in prolactin and plasma cortisol release. Citalopram is a racemic mixture of equal proportions of the S(+) and R(-) enantiomers. Inhibition of serotonin reuptake and, consequently, antidepressant activity is associated, almost exclusively, with the S(+) enantiomer ("escitalopram"). Studies in animal models indicate that the presence of the R(-) isomer may interfere with the serotonin reuptake activity of escitalopram. The current study compared the neuroendocrine effects of citalopram and escitalopram in healthy human volunteers. Plasma cortisol and prolactin levels following a single oral dose of citalopram (40 mg) or escitalopram (20 mg) were compared in samples taken every 15-30 min over a period of 240 min. Plasma citalopram concentration was determined at the same intervals. Escitalopram and citalopram caused equivalent increases in plasma cortisol and prolactin. The administration of dexamethasone prior to the escitalopram challenge blocked the evoked increase in cortisol. This is the first study to prove that a single dose of escitalopram acts centrally and not peripherally, providing further support of the use of oral escitalopram as a probe for brain serotonergic function.