Serotonin release from platelets and polymorphonuclear leukocytes

Serotonin release from platelets and polymorphonuclear leukocytes refers to a physiological process and functional assay endpoint rather than a single molecular target. Platelets sequester serotonin (5-HT) from the plasma via the serotonin transporter (SERT/SLC6A4) and store it in dense granules at high concentrations (Sari et al., 2010, PMC2917125). Upon activation by stimuli like thrombin or collagen, platelets undergo degranulation, releasing serotonin to facilitate vasoconstriction and accelerate further platelet aggregation through 5-HT2A receptor signaling (Vanhoutte, 1991, PubMed: 18391166). While polymorphonuclear leukocytes (PMNs) are primarily immune effectors, they interact closely with platelets during inflammatory responses, and this crosstalk can modulate the release of various bioactive substances, including serotonin, which acts as a bridge between hemostasis and innate immunity (Zarbock et al., 2007, Journal of Leukocyte Biology). Pharmacological modulation of this process is primarily achieved through Selective Serotonin Reuptake Inhibitors (SSRIs), which deplete platelet serotonin stores, or through 5-HT2A receptor antagonists (Hergovich et al., 2002, Arteriosclerosis, Thrombosis, and Vascular Biology). Consequently, this process is frequently monitored in clinical and research settings as a biomarker for platelet function and the efficacy of antithrombotic or antidepressant therapies.

Other names

Platelet serotonin secretion5-HT release from blood cellsPlatelet degranulationSerotonin release assay

Drugs typically modulate this process by inhibiting the serotonin transporter (SERT) to deplete intracellular stores or by blocking receptors such as 5-HT2A that trigger degranulation.