| First Author | Jadavji NM | Year | 2015 |
| Journal | Mol Genet Metab Rep | Volume | 3 |
| Pages | 1-4 | PubMed ID | 26937386 |
| Mgi Jnum | J:290577 | Mgi Id | MGI:6444021 |
| Doi | 10.1016/j.ymgmr.2015.02.001 | Citation | Jadavji NM, et al. (2015) Methylenetetrahydrofolate reductase deficiency alters levels of glutamate and gamma-aminobutyric acid in brain tissue. Mol Genet Metab Rep 3:1-4 |
| abstractText | 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 gamma-aminobutyric acid in within the cerebellum and hippocampus. Mthfr (-/-) mice had reduced levels of glutamate in the amygdala and gamma-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 gamma-aminobutyric acid. |
