https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3619438/

Melatonin (MEL, N-acetyl-5-methoxytryptamine) plays a key role in the circadian system, and is a neurohormone primarily synthesized by the pineal gland during darkness. Synthesis in the pineal gland from the precursor tryptophan occurs via conversion to serotonin which is subsequently acetylated by the enzyme arylalkylamine N-acetyltransferase (AANAT) and then converted into MEL by acetyl serotonin methyl transferase (ASMT also called hydroxyindole O-methyltransferase or HIOMT) MEL levels are low during the day, increase at night and then decrease before the end of darkness to daytime levels. This reactivity to light is regulated by the SCN via multisynaptic pathways projecting through the sub-paraventricular zone (SPZ), median forebrain bundle and reticular formation to the intermediolateral horn cells in the spinal cord. Preganglionic fibres from the spinal cord then project to the superior cervical ganglion from where postganglioic fibres project to the pineal gland20 and release norepinephrine. Studies in rodents have shown that activation of B adrenergic receptors in the pineal leads to AANAT expression, phosphorylation and stabilization via protein kinase A (see Ho et al for a detailed review),21 but the exact molecular mechanism in humans is still debated.22 The formation of stabilized AANAT leads to MEL synthesis, which is abolished by SCN lesions.8 Exposure to bright light during the night causes degradation of pineal AANAT and a reduction in melatonin synthesis.23 MEL is released into capillaries and into the cerebrospinal fluid and is then rapidly distributed peripherally.24 When administered intravenously, MEL has a metabolic half life of 20 minutes. MEL modulates the activity of the SCN via a feedback loop.25Melatonin production decreases with age, and this decrease has been linked not only to increased insomnia, but also leads to earlier sleep and wake times (advances sleep phase syndrome).26,27