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. 2021 Apr 8;12:638981. doi: 10.3389/fpsyt.2021.638981

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Copyright © 2021 Tonon, Pilz, Markus, Hidalgo and Elisabetsky.

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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The canonical pathway of pineal melatonin production. The suprachiasmatic nucleus (SCN) receives environmental photic information collected by intrinsically photosensitive ganglion cells (ipRGC) in the retina. The ipRGCs express the photopigment melanopsin, which transduces light wavelengths into neural input through the retinohypothalamic tract (RHT) to the SCN. The SCN constitutively inhibits the hypothalamic paraventricular nucleus (PVN) via GABAergic projection. In the absence of light, the PVN activates the ganglion cervical nuclei (SCG, via the intermediolateral column of the medulla) triggering noradrenergic fibers that innervate the pineal gland (PG), ultimately releasing the co-transmitters noradrenaline and ATP. This sympathetic stimulus triggers the action of arylalkylamine N-acetyltransferase (AANAT) converting serotonin (5TH) into N-acetylserotonin (NAS) within the pinealocyte. With the constitutive action of N-acetylserotonin O-methyltransferase (ASMT), NAS is then converted to melatonin and immediately released into the cerebrospinal fluid and bloodstream. Through first-pass metabolism in the liver, melatonin is converted to 6-sulfatoxymelatonin (aMT6s), which is then excreted in the urine.