@article{oai:niigata-u.repo.nii.ac.jp:00014658, author = {柿崎, 利和}, issue = {10}, journal = {新潟医学会雑誌, 新潟医学会雑誌}, month = {Oct}, note = {The N -methyl-D-aspartate (NMDA) subtype of the glutamate receptor (GluR) channel plays roles in synaptic plasticity as a molecular coincident detector and in neuronal pattern formation during development. NMDA receptor channels are composed of the GluRε (NR 2) and GluRζ (NR 1) subunits. There are four GluRε subunit genes, although GluRζ subunit variants are derived from a single gene. The molecular composition of NMDA receptor channels varies depending on the location and developmental stage of brain. At the embryonic stage, GluRε 2 mRNA is expressed in the entire brain, while GluRε 4 mRNA is expressed only in the diencephalon and brainstem. Therefore, I focused on the GluRε 2 and GluRε 4 subunits to determine their functions during development. I produced a mutant mouse line (ε 4-E2), which expressed GluRε 2 protein under the GluRε 4 gene promoter, by inserting ε 2 cDNA into GluRε 4 subunit gene with the homologous recombination. In this mutant mice, I found GluRε 2 appeared instead of GluRε 4, and compared its behavioral phenotype with that of the GluRε 4 knockout mouse. Theε 4-E2 mutant mice showed a significantly lower spontaneous activity than that of the GluRε 4 knockout mice. On the other hand, there was no significant difference in the spontaneous activity between the GluRε 4 mutant mice and wild-type mice. These results suggest that the GluRε 2 and GluRε 4 are distinct in functional properties and GluRε 2 cannot compensate the function of GluRε 4.}, pages = {518--527}, title = {脳発達時期に発現するNMDA受容体チャネルε2, ε4サブユニットの機能的差違}, volume = {115}, year = {2001} }