Department of Biological Sciences, Konkuk University, Seoul 143-701, Korea.
Mol Cells. 2013 Aug;36(2):99-104. doi: 10.1007/s10059-013-0113-y. Epub 2013 Jun 4.
Recent reports have proposed a novel function for the N-methyl-D-aspartate (NMDA) receptor (NMDAR), a well-known excitatory, ionotropic receptor. A series of observations employing pharmacological techniques has proposed that upon ligand binding, this ionotropic receptor can actually function via signaling cascades independent of traditional ionotropic action. Moreover, the "metabotropic" action of NMDARs is suggested to mediate a form of synaptic plasticity, namely long-term synaptic depression (LTD), which shares cellular mechanisms with the synaptic deficits observed in Alzheimer's disease. Given that a growing body of clinical and preclinical evidence strongly recommends NMDAR antagonists for their therapeutic potentials and advantages in a variety of diseases, further investigation into their molecular and cellular mechanisms is required to better understand the "metabotropic" action of NMDARs.
最近的报告提出了 N-甲基-D-天冬氨酸（NMDA）受体（NMDAR）的一种新功能，NMDAR 是一种众所周知的兴奋性离子型受体。一系列采用药理学技术的观察结果表明，配体结合后，这种离子型受体实际上可以通过独立于传统离子型作用的信号级联发挥作用。此外，NMDAR 的“代谢型”作用被认为介导了一种形式的突触可塑性，即长时程突触抑制（LTD），它与阿尔茨海默病中观察到的突触缺陷具有相同的细胞机制。鉴于越来越多的临床和临床前证据强烈推荐 NMDAR 拮抗剂具有治疗潜力和多种疾病的优势，因此需要进一步研究其分子和细胞机制，以更好地理解 NMDAR 的“代谢型”作用。
