Platelets in psychiatric disorders

Figure 1 In the vessel wall an intact endothelium prevents platelet activation, adhesion, as well as aggregation by producing prostacyclin and nitric oxide favoring quiescent platelets (blue spheres). A damaged endothelium, a platelet agonist [thrombin, fibrinogen, vonWillebrandt factor (vWF), collagen, adrenalin], shear stress or the coagulation process itself can induce platelet activation. During this process a rise in intracellular calcium (Ca²⁺) levels lead to shape change, where the platelet membrane surface area is greatly increased (black irregular spheres). This is accompanied by the release/secretion of various substances [e.g., adenosine-di- and triphosphate (ADP/ATP), Ca²⁺, magnesium (Mg²⁺), platelet derived growth factor (PDGF), serotonin, transforming growth factor-β (TGF-β), fibrinogen, platelet factor-4] from the platelets specialized α and dense granules. The adhesion of platelets is induced under conditions of high shear stress, by exposure to a platelet agonist (e.g., collagen, vWF) or follows the activation process resulting in platelets aggregation and blood clotting. All these processes are Ca²⁺ and Mg²⁺ dependent. PGI₂: Producing prostacyclin; NO: Nitric oxide.