To the Editor.—
Alcoholic patients have lower levels of 5-hydroxyindoleacetic acid in cerebrospinal fluid1; decreased availability of the serotonin precursor, tryptophan2; and reduced serotonin concentrations in platelets.3 These findings have led to the hypothesis that a dysregulation in serotonin metabolism may be involved in the pathogenesis of alcoholism. To further explore this hypothesis, we studied alcoholic patients who abstained from alcohol. Behavioral, physiological, and endocrine responses to the metabolite of trazodone hydrochloride, meta-chlorophenylpiperazine (m-CPP) hydrochloride, were used as indexes of serotonin receptor function in alcoholic patients.4Twenty-one male patients who fulfilled DSM-III-R criteria for alcohol dependence and Research Diagnostic Criteria for alcoholism were selected for the study. They were in good physical health, euthymic, and abstinent from alcohol for at least 3 weeks when the study began. After written, informed consent was obtained, normal saline solution (the placebo) was administered intravenously. Thirty minutes later, m-CPP (0.08
Benkelfat C, Murphy DL, Hill JL, George DT, Nutt D, Linnoila M. Ethanollike Properties of the Serotonergic Partial Agonist m-Chlorophenylpiperazine in Chronic Alcoholic Patients. Arch Gen Psychiatry. 1991;48(4):383. doi:10.1001/archpsyc.1991.01810280099018
* * SCHEDULED MAINTENANCE * *
The JAMA Network Sites will be conducting routine maintenance from 10/20/2017 through 10/21/2017. During this window access to content and authentication may be intermittently available. The JAMA Store will be completely unavailable during the maintenance window.