N-Acetylputrescine
Endogenous GABA precursor
From Wikipedia, the free encyclopedia
N-Acetylputrescine (NacPut), also known as monoacetylputrescine, is an endogenous metabolite of putrescine and a precursor and metabolic intermediate in the biosynthesis of γ-aminobutyric acid (GABA) from putrescine.[1][2][3]
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| Names | |
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| IUPAC name
N-(4-aminobutyl)acetamide | |
| Other names
Acetylputrescine; Monoacetylputrescine; NacPut | |
| Identifiers | |
3D model (JSmol) |
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| ChEMBL | |
| ChemSpider | |
| ECHA InfoCard | 100.219.140 |
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| KEGG | |
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| UNII | |
CompTox Dashboard (EPA) |
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| Properties | |
| C6H14N2O | |
| Molar mass | 130.19 g/mol |
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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The metabolic pathway is specifically putrescine into N-acetylputrescine by putrescine acetyltransferase (PAT), N-acetylputrescine into N-acetyl-γ-aminobutyraldehyde (N-acetyl-GABAL or N-acetyl-GABA aldehyde) by monoamine oxidase B (MAO-B), N-acetyl-GABAL into N-acetyl-γ-aminobutyric acid (N-acetyl-GABA) by aldehyde dehydrogenase (ALDH), and N-acetyl-GABA into GABA by an unknown deacetylase enzyme.[1][2][3] This pathway is a minor alternative pathway to the major and primary pathway in which GABA is synthesized from glutamate.[1] There is also another alternative pathway in which putrescine is converted into GABA with γ-aminobutyraldehyde (GABAL or GABA aldehyde) as an intermediate instead.[1] It has been estimated that about 2 to 3% of GABA is synthesized from putrescine in the mouse brain, whereas in the case of the rat brain, the amount was negligible.[1]
In 2021, it was discovered that MAO-B does not mediate dopamine catabolism in the rodent striatum but instead participates in striatal GABA synthesis and that synthesized GABA in turn inhibits dopaminergic neurons in this brain area.[4][3] It has been found that MAO-B, via the putrescine pathway, importantly mediates GABA synthesis in astrocytes in various brain areas, including in the hippocampus, cerebellum, striatum, cerebral cortex, and substantia nigra pars compacta (SNpc).[4][3] These findings may warrant a rethinking of the actions of MAO-B inhibitors in the treatment of Parkinson's disease.[4][3]
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