Huettner J E
Department of Neurobiology, Harvard Medical School, Boston, MA 02115.
Science. 1989 Mar 24;243(4898):1611-3. doi: 10.1126/science.2467381.
The N-methyl-D-aspartate (NMDA) class of excitatory amino acid receptors regulates the strength and stability of excitatory synapses and appears to play a major role in excitotoxic neuronal death associated with stroke and epilepsy. The conductance increase gated by NMDA is potentiated by the amino acid glycine, which acts at an allosteric site tightly coupled to the NMDA receptor. Indole-2-carboxylic acid (I2CA) specifically and competitively inhibits the potentiation by glycine of NMDA-gated current. In solutions containing low levels of glycine, I2CA completely blocks the response to NMDA, suggesting that NMDA alone is not sufficient for channel activation. I2CA will be useful for defining the interaction of glycine with NMDA receptors and for determining the in vivo role of glycine in excitotoxicity and synapse stabilization.
N-甲基-D-天冬氨酸（NMDA）类兴奋性氨基酸受体调节兴奋性突触的强度和稳定性，并且似乎在与中风和癫痫相关的兴奋性毒性神经元死亡中起主要作用。由NMDA控制的电导增加被氨基酸甘氨酸增强，甘氨酸作用于与NMDA受体紧密偶联的变构位点。吲哚-2-羧酸（I2CA）特异性地且竞争性地抑制甘氨酸对NMDA门控电流的增强作用。在含有低水平甘氨酸的溶液中，I2CA完全阻断对NMDA的反应，这表明仅NMDA不足以激活通道。I2CA将有助于确定甘氨酸与NMDA受体的相互作用，并有助于确定甘氨酸在兴奋性毒性和突触稳定中的体内作用。
