['Central nervous system serotonergic neurotransmission appears to play a role in mood disorders, eating habits, and sleep, and also modulates blood pressure and metabolism. This investigation tested a hypothesized association between central serotonergic functioning and preclinical atherosclerosis.', 'Subjects were 244 adults 30 to 55 years of age and free of clinically evident vascular disease (52% men, 84% white). Central serotonergic responsivity was measured as the rise in serum prolactin concentration (area under the curve) over 2.5 hours, adjusted for baseline prolactin, after citalopram administered intravenously at 0.33 mg/kg lean body weight. Carotid artery morphology served as a marker of preclinical atherosclerosis, and carotid artery intima-media thickness and plaque occurrence were determined by B-mode ultrasonography.', 'In linear regression models including age, gender, race, and citalopram concentration, a 1 SD lower prolactin response was associated with greater maximum intima-media thickness (+0.016 mm; P=0.006) and with greater mean intima-media thickness (+0.009 mm; P=0.03). The odds ratio for carotid artery plaque corresponding to a 1 SD decrease in prolactin response, adjusted for age, race, sex, and citalopram concentration, was 1.47 (95% CI, 0.98 to 2.19; P=0.06). The metabolic syndrome mediated (P<0.01), but did not fully account for, the association between lower prolactin response and greater maximum intima-media thickness.'] Is lower central serotonergic responsivity associated with preclinical carotid artery atherosclerosis?