Ishiwata Sayuri, Umino Asami, Balu Darrick T, Coyle Joseph T, Nishikawa Toru
Department of Psychiatry and Behavioral Sciences, Graduate School of Medical and Dental Sciences, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo, 113-8519, Japan.
J Neural Transm (Vienna). 2015 Aug;122(8):1099-103. doi: 10.1007/s00702-015-1388-2. Epub 2015 Mar 18.
In the hippocampus of mice lacking the gene for serine racemase (SR), a D-serine synthesizing enzyme, in the CaMKIIα-expressing neurons, we observed a significant decrease in the extracellular concentration of D-serine, a coagonist for the N-methyl-D-aspartate type glutamate receptor (NMDAR), and NMDAR hypofunction as revealed by diminished extracellular taurine concentrations after an intra-hippocampal NMDA infusion when compared to the wild type controls. Therefore, the neuronal SR could regulate the extracellular D-serine signaling responsible for NMDAR activation in the hippocampus.
在缺乏丝氨酸消旋酶(SR,一种D-丝氨酸合成酶)基因的小鼠海马体中,在表达CaMKIIα的神经元中,我们观察到D-丝氨酸(N-甲基-D-天冬氨酸型谷氨酸受体(NMDAR)的一种协同激动剂)的细胞外浓度显著降低,并且与野生型对照相比,海马体内注入NMDA后细胞外牛磺酸浓度降低,这表明NMDAR功能减退。因此,神经元SR可能调节负责海马体中NMDAR激活的细胞外D-丝氨酸信号传导。