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Fluoxetine,
but not tricyclic antidepressants, potentiates the 5-hydroxytryptophan-mediated
increase in plasma cortisol and prolactin secretion in subjects with major
depression or with obsessive compulsive disorder.
Meltzer H, Bastani B, Jayathilake K, Maes M.
Department of Psychiatry, Vanderbilt University School of Medicine, Nashville,
Tennessee, USA.
It has been suggested that the clinical efficacy of chronic treatment with
selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine and perhaps
all antidepressants is due to their ability to enhance serotonergic activity. The
effects of chronic treatment with fluoxetine or tricyclic antidepressants on
the L-5-hydroxytryptophan (200 mg, L-5-HTP; PO)-induced increases in plasma
cortisol and prolactin (PRL) concentrations were studied in patients with major
depression or obsessive compulsive disorder (OCD). Administration of L-5-HTP
increased plasma cortisol and PRL levels in medicated and unmedicated patients
with major depression or OCD. The L-5-HTP-induced cortisol and PRL responses
were significantly higher in fluoxetine-treated than in tricyclic-treated or
unmedicated major depressed patients. The latter two groups did not differ
significantly in their cortisol or PRL responses to L-5-HTP. The
L-5-HTP-induced increases in cortisol and PRL in fluoxetine-treated patients
with major depression or OCD were not significantly different. The results
suggest that fluoxetine, but not tricyclic antidepressants, potentiates 5-HT
receptor-mediated stimulation of cortisol and PRL secretion in humans,
consistent with available evidence that fluoxetine treatment, but not tricyclic
antidepressants, increases central serotonergic activity in patients with MD or
OCD by a presynaptic mechanism.
Publication Types:
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Clinical
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Controlled
Clinical Trial
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