N-Acetyl-5-hydroxytryptamineN-

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N-Acetyl-5-hydroxytryptamine

CAS No. : 1210-83-9

MCE 国际站：N-Acetyl-5-hydroxytryptamine

产品活性：N-Acetyl-5-hydroxytryptamine 是褪黑激素前体，可有效地激活 TrkB 受体。

研究领域：Metabolic Enzyme/Protease  |  Protein Tyrosine Kinase/RTK  |  Neuronal Signaling

作用靶点：Endogenous Metabolite  |  Trk Receptor

结构分类：酚类  |  单酚类  |  生物碱  |  吲哚类生物碱

In Vitro: N-Acetyl-5-hydroxytryptamine (NAS), a precursor of Melatonin, is acetylated from serotonin by AANAT (arylalkylamine N-acetyltransferase). N-acetylserotonin activates TrkB receptor in a circadian rhythm. N-Acetyl-5-hydroxytryptamine swiftly activates TrkB in a circadian manner and exhibits antidepressant effect in a TrkB-dependent manner. N-Acetyl-5-hydroxytryptamine rapidly activates TrkB, but not TrkA or TrkC, in a neurotrophin- and MT3 receptor-independent manner.

In Vivo: To explore whether N-Acetyl-5-hydroxytryptamine, can trigger TrkB activation in vivo, TrkB F616A knockin mice are employed, where it has been shown that TrkB F616A activation can be selectively blocked by 1NMPP1, a derivative of kinase inhibitor PP1, leading to TrkB-null phenotypes. To assess whether N-Acetyl-5-hydroxytryptamine can mimic BDNF, cortical neurons from TrkB F616A knockin mice are prepared. In alignment with a previous report, BDNF- and NAS-mediated TrkB phosphorylation are selectively reduced by 1NMPP1 but not by K252a, whereas serotonin or Melatonin had no effect . These findings suggest that NAS strongly provokes both wild-type TrkB and TrkB F616A tyrosine phosphorylation and activation.

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