Nishijima K, Kashiwa A, Nishikawa T
Department of Mental Disorder Research, National Institute of Neuroscience, Tokyo, Japan.
J Neurochem. 1994 Jul;63(1):375-8. doi: 10.1046/j.1471-4159.1994.63010375.x.
Using a brain microdialysis technique, we have shown in the rat that local infusion of a selective and competitive N-methyl-D-aspartate (NMDA) receptor antagonist, cis-4-phosphonomethyl-2-piperidine carboxylic acid (CGS-19755), into the medial frontal cortex via dialysis tubing caused a concentration-related increase in the extracellular release of dopamine, 3,4-dihydroxyphenylacetic acid, and homovanillic acid in the cortical region. Coinfusion of a sodium channel blocker, tetrodotoxin, completely inhibited the ability of the NMDA antagonist to augment frontal dopamine metabolism. These findings suggest that dopamine neurons projecting to the frontal cortex might be under a tonic transsynaptic inhibition exerted by excitatory amino acid neurotransmission via the NMDA receptor at the level of dopamine terminal fields.
运用脑微透析技术，我们在大鼠实验中发现，通过透析管向内侧额叶皮质局部注入选择性竞争性N-甲基-D-天冬氨酸（NMDA）受体拮抗剂顺式-4-膦酰甲基-2-哌啶甲酸（CGS-19755），会导致皮质区域细胞外多巴胺、3,4-二羟基苯乙酸和高香草酸的释放量随浓度增加。同时注入钠通道阻滞剂河豚毒素，可完全抑制NMDA拮抗剂增强额叶多巴胺代谢的能力。这些发现表明，投射至额叶皮质的多巴胺神经元可能在多巴胺终末场水平受到兴奋性氨基酸通过NMDA受体进行的紧张性跨突触抑制。
