Chemistry:N-Acetylputrescine

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Short description: Endogenous GABA precursor


N-Acetylputrescine
Names
IUPAC name
N-(4-aminobutyl)acetamide
Other names
Acetylputrescine; Monoacetylputrescine; NacPut
Identifiers
3D model (JSmol)
ChEBI
ChEMBL
ChemSpider
EC Number
  • 691-457-0
KEGG
UNII
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).
Infobox references

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]

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]

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 "GABA and GABA Receptors in the Central Nervous System and Other Organs". A Survey of Cell Biology. International Review of Cytology. 213. 2002. pp. 1–47. doi:10.1016/s0074-7696(02)13011-7. ISBN 978-0-12-364617-0. 
  2. ↑ 2.0 2.1 "Catabolism of polyamines". Amino Acids 26 (3): 217–233. June 2004. doi:10.1007/s00726-004-0070-z. PMID 15221502. 
  3. ↑ 3.0 3.1 3.2 3.3 3.4 "Redefining differential roles of MAO-A in dopamine degradation and MAO-B in tonic GABA synthesis". Exp Mol Med 53 (7): 1148–1158. July 2021. doi:10.1038/s12276-021-00646-3. PMID 34244591. 
  4. ↑ 4.0 4.1 4.2 "Revisiting the Role of Astrocytic MAOB in Parkinson's Disease". Int J Mol Sci 23 (8): 4453. April 2022. doi:10.3390/ijms23084453. PMID 35457272. 

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See also
Receptor/signaling modulators
GABAA receptor positive modulators
GABA metabolism/transport modulators

}}




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