Methylenetetrahydrofolate reductase deficiency alters levels of glutamate and γ-aminobutyric acid in brain tissue.
Mol Genet Metab Rep
; 3: 1-4, 2015 Jun.
Article
em En
| MEDLINE
| ID: mdl-26937386
ABSTRACT
Methylenetetrahydrofolate reductase (MTHFR) is an enzyme key regulator in folate metabolism. Deficiencies in MTHFR result in increased levels of homocysteine, which leads to reduced levels of S-adenosylmethionine (SAM). In the brain, SAM donates methyl groups to catechol-O-methyltransferase (COMT), which is involved in neurotransmitter analysis. Using the MTHFR-deficient mouse model the purpose of this study was to investigate levels of monoamine neurotransmitters and amino acid levels in brain tissue. MTHFR deficiency affected levels of both glutamate and γ-aminobutyric acid in within the cerebellum and hippocampus. Mthfr (-/-) mice had reduced levels of glutamate in the amygdala and γ-aminobutyric acid in the thalamus. The excitatory mechanisms of homocysteine through activation of the N-methyl-d-aspartate receptor in brain tissue might alter levels of glutamate and γ-aminobutyric acid.
5-HIAA, 5-hydroxyindoleacetic acid; 5-HT, serotonin.; 5-methylTHF, 5-methyltetrahydrofolate; COMT, catechol-O-methyltransferase; DOPAC, 3,4-dihydroxyphenylacetic acid; GABA, γ-aminobutyric acid; Glutamate; HPLC, high performance liquid chromatography; HVA, homovanillic acid; Homocysteine; MTHFR, methylenetetrahydrofolate reductase; Methylenetetrahydrofolate reductase; Monoamine neurotransmitters; S-Adenosylmethionine; SAM, S-adenosylmethionine; γ-Aminobutyric acid
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Coleções:
01-internacional
Base de dados:
MEDLINE
Idioma:
En
Ano de publicação:
2015
Tipo de documento:
Article