The role of the N-Methyl-D-Aspartate Receptor (NMDAR) in the outer retina is unclear despite expression of the NMDAR-complex and its subunits in the outer retina. The flash-electroretinogram (fERG) offers a non-invasive measurement of the retinal field potentials of the outer retina that can serve to clarify NMDAR contribution to early retinal processing. The role of the NMDAR in retinal function was assessed using a genetic mouse model for NMDAR hypofunction (SR^-/-), where the absence of the enzyme serine racemase (SR) results in an 85% reduction of retinal D-serine. NMDAR hypo- and hyperfunction in the retina results in alterations in the components of the fERG. The fERG was examined after application of exogenous D-serine to the eye in order to determine whether pre- and post-topical delivery of D-serine would alter the fERG in SR^-/- mice and their littermate WT controls. Amplitude and implicit time of the low-frequency components, the a- and b-wave, were conducted. Reduced NMDAR function resulted in a statistically significantly delayed a-wave and reduced b-wave in SR^-/- animals. The effect of NMDAR deprivation was more prominent in male SR^-/- mice. A hyperfunction of the NMDAR, through exogenous topical delivery of 5 mM D-serine, in WT mice caused a significantly delayed a-wave implicit time and reduced b-wave amplitude. These changes were not observed in female WT mice. There were temporal delays in the a-wave and amplitude and a decrease in the b-wave amplitude and implicit time in both hypo- and NMDAR hyperfunctional male mice. These results suggest that NMDAR and D-serine are involved in the retinal field potentials of the outer retina that interact based on the animal's sex. This implicates the involvement of gonadal hormones and D-serine in retinal functional integrity.

尽管 NMDAR 复合物及其亚基在外层视网膜中表达，但 N-甲基-D-天冬氨酸受体 (NMDAR) 在外层视网膜中的作用尚不清楚。闪光视网膜电图 (fERG) 提供了对外部视网膜的视网膜场电位的非侵入性测量，可用于阐明 NMDAR 对早期视网膜处理的贡献。NMDAR 在视网膜功能中的作用使用 NMDAR 功能减退的遗传小鼠模型进行评估 (SR ^-/-)，其中丝氨酸消旋酶 (SR) 的缺失导致视黄醛 D-丝氨酸减少 85%。视网膜中的 NMDAR 功能减退和功能亢进导致 fERG 成分的改变。在将外源 D-丝氨酸应用于眼睛后检查 fERG，以确定 D-丝氨酸的局部前和局部递送是否会改变 SR ^{- /-}小鼠及其同窝 WT 对照中的 fERG。进行了低频分量 a 波和 b 波的幅度和隐含时间。NMDAR 功能降低导致 SR ^{- /-}动物的 a 波和 b 波在统计学上显着延迟。NMDAR 剥夺对男性 SR 的影响更为突出^{- /-}老鼠。NMDAR 的机能亢进，通过外源性局部递送 5 mM D-丝氨酸，在 WT 小鼠中导致显着延迟的 a 波隐含时间和降低的 b 波振幅。在雌性 WT 小鼠中未观察到这些变化。在低功能和 NMDAR 功能亢进的雄性小鼠中，a 波和振幅存在时间延迟，b 波振幅和隐含时间减少。这些结果表明，NMDAR 和 D-丝氨酸参与了基于动物性别相互作用的外层视网膜的视网膜场电位。这暗示性腺激素和 D-丝氨酸参与视网膜功能完整性。