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Like melatonin, NAS is an agonist at the melatonin receptorsMT1, MT2, and MT3, and may be considered to be a neurotransmitter. In addition, NAS is distributed in some areas of the brain where serotonin and melatonin are not, suggesting that it may have unique central duties of its own instead of merely functioning as a precursor in the synthesis of melatonin. NAS is known to have anti-depressant, neurotrophic and cognition-enhancing effects and has been proposed to be a target for the treatment of aging-associated cognitive decline and depression
TrkB receptor
NAS has been shown to act as a potentTrkB receptor agonist, while serotonin and melatonin do not. Subchronic and chronic administration of NAS to adult mice induces proliferation of neural
progenitor cells (NPC)s, blockage of TrkB abolished this effect suggesting that it is TrkB-dependent. NAS was also found to significantly enhance NPC proliferation in sleep-deprived mice. It is thought that the anti-depressant and neurotrophic effects of NAS are in part due to its role as a TrkB agonist.
Antioxidant properties
NAS acts as a potent antioxidant, NAS effectiveness as an anti-oxidant has been found to be different depending on the experimental model used, it has been described as being between 5 and 20 times more effect than melatonin at protecting against oxidant damage. NAS has been shown to protect against lipid peroxidation in microsomes and mitochondria. NAS has also been reported to lower resting levels of ROS in peripheral blood lymphocytes and to exhibit anti-oxidant effects against t-butylated hydroperoxide- and diamide-induced ROS. NAS has also been observed to inhibit nitric oxide synthase.
NAS may play a role in the antidepressant effects of selective serotonin reuptake inhibitors (SSRIs) and monoamine oxidase inhibitors (MAOIs). The SSRI fluoxetine and the MAO-Ainhibitorclorgylineupregulate AANAT indirectly through serotonergic mechanisms and thereby increase NAS levels after chronic administration, and this correlates with the onset of their antidepressant effects. Furthermore, light exposure inhibits the synthesis of NAS and reduces the antidepressant effects of MAOIs. In addition, AANAT knockout mice display significantly greater immobility times versus control mice in animal models of depression. These data support a potential role for NAS in mood regulation and in antidepressant-induced therapeutic benefits.
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