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. 2021 Nov 30;12:771144. doi: 10.3389/fpsyt.2021.771144

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Copyright © 2021 Ansarey.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Niacin binds and activates GPR109A receptors on dermal cells, epidermal langerhans cells, and adipose macrophages (27). In langerhans cells, the activated receptor releases intracellular calcium (Ca²⁺) (28), which triggers phospholipase A₂ (PLA₂) to catalyse the breakdown of membrane phospholipid to arachidonic acid (AA). Available AA is converted to eicosanoid, prostaglandin G₂ (PGG₂) and prostaglandin H₂ (PGH₂) via COX1/2 and hydrogen peroxidase respectively. PGH₂ is converted to various prostaglandins, prostacyclins, and leukotrienes. However, because this thesis focuses on the diminished flush observed in schizophrenia, I will focus on prostaglandins (29). Mediators involved in the cutaneous flushing are vasodilators, prostaglandin D2 (PGD₂), and E2 (PDE₂), which activates prostaglandin D₂ receptor 1 (DP₁) and prostaglandin E_2/4 receptor (EP_2/4), respectively (25). Moreover, these are biochemical alteration which may be partially inherited (30, 31). However, the pathophysiology of the attenuated flush response is not fully understood.