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-dependant. 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.
NAS acts as a potent anti-oxidant, 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 to 20 times more effect then 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.
^ abTosini G., Ye K. & Iuvone PM. (2012) neuroprotection, neurogenesis, and the sleepy brain. Neuroscientist, 18(6):645-53.
^ abOxenkrug G. & Ratner R. (2012) N-acetylserotonin and aging-associated cognitive impairment and depression. Aging Dis., 3(4):330-8.
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^ abOxenkrug GF (1997). "[N-acetylserotonin and hypotensive effect of MAO-A inhibitors]". Voprosy Meditsinskoi Khimii (in Russian) 43 (6): 522–6. PMID9503569.
^Sompol P., Liu X., Baba K., Paul KN., Tosini G., Iuvone PM. & Ye K. (2011) N-acetylserotonin promotes hippocampal neuroprogenitor cell proliferation in sleep-deprived mice. Proc. Natl. Acad. Sci. U. S. A., 108(21):8844-9.