While citalopram pharmacology has been extensively investigated and defined, the molecular mechanisms underlying brain functional response to this antidepressant are less well characterised. Therefore, we explored the functional response of the healthy brain to an acute citalopram challenge by enriching resting-state fMRI with molecular templates of serotonin neurotransmitters. We found that a high oral dose of citalopram induces significant alterations in 5-HT1A-enriched functional connectivity, and that serotonin transporter occupancy is linked with the interindividual functional response to citalopram in the SERT-related network. These findings set a new basis for a mechanistic understanding of the functional effects of citalopram in depression.
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