Jadavji N M, Wieske F, Dirnagl U, Winter C
Department of Experimental Neurology, Center for Stroke Research Berlin, Charité University Medicine Berlin, Germany.
Department of Experimental Psychiatry, University Hospital Carl Gustav Carus, Technische Universitaet Dresden, Dresden, Germany.
Mol Genet Metab Rep. 2015 Feb 20;3:1-4. doi: 10.1016/j.ymgmr.2015.02.001. eCollection 2015 Jun.
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.
亚甲基四氢叶酸还原酶（MTHFR）是叶酸代谢中的一种关键酶调节因子。MTHFR缺乏会导致同型半胱氨酸水平升高，进而导致S-腺苷甲硫氨酸（SAM）水平降低。在大脑中，SAM将甲基基团提供给儿茶酚-O-甲基转移酶（COMT），后者参与神经递质分析。本研究利用MTHFR缺陷小鼠模型，旨在研究脑组织中单胺神经递质水平和氨基酸水平。MTHFR缺乏影响小脑和海马体内谷氨酸和γ-氨基丁酸的水平。Mthfr（-/-）小鼠杏仁核中的谷氨酸水平和丘脑中的γ-氨基丁酸水平降低。同型半胱氨酸通过激活脑组织中的N-甲基-D-天冬氨酸受体产生的兴奋机制可能会改变谷氨酸和γ-氨基丁酸的水平。
