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The Serotonin Transporter Modulates the Kinetics and Quantal Size of Vesicular Fusion Events in Sympathoadrenal Chromaffin Cells

The antidepressant‐sensitive serotonin transporter (SERT) is a key regulator of serotonin (5‐HT) signaling and availability in the CNS. The robust expression of SERT in adrenal chromaffin cells (ACCs), which comprise the neuroendocrine arm of the sympathetic nervous system, is less well understood. ACCs synthesize and secrete catecholamines (epinephrine, norepinephrine) which mediate the physiological response to stress. They do not synthesize 5‐HT, but do accumulate small amounts through SERT‐mediated uptake (5‐HT content is <0.15% of the epinephrine content). We hypothesized that the chromaffin cells utilize this 5‐HT for autocrine / paracrine control of the sympathoadrenal stress response. Consistent with this hypothesis, we previously reported that 5‐HT1A receptors inhibit catecholamine secretion by reducing the number of secretory vesicles that fuse with the plasma. The objective of the current study was to investigate an additional, receptor‐independent mechanism by which SERT controls adrenal catecholamine secretion.