Ohno M, Arai I, Watanabe S
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Brain Res. 1995 Nov 20;699(2):332-5. doi: 10.1016/0006-8993(95)01086-b.
Intracerebral microdialysis technique was utilized to study the effect of NG-nitro-L-arginine, a nitric oxide (NO) synthase inhibitor, on N-methyl-D-aspartate (NMDA)-induced dopamine overflow in the nucleus accumbens of unanesthetized, freely moving rats. Perfusion of 1 and 3 mM NMDA through the microdialysis probe dose-dependently increased the extracellular dopamine level in the nucleus accumbens. Coapplication of 0.5 mM D-(-)-2-amino-5-phosphonovaleric acid (D-AP5), a selective and competitive NMDA receptor antagonist, significantly reduced the dopamine overflow induced by 3 mM NMDA. Perfusion of 0.5 mM NG-nitro-L-arginine alone did not affect the basal dopamine level, whereas it suppressed the NMDA-evoked dopamine overflow in the nucleus accumbens when concurrently applied with 3 mM NMDA. These results suggest that NO mediates, at least in part, dopamine release resulting from NMDA receptor activation in the nucleus accumbens of rats.
采用脑内微透析技术，研究一氧化氮（NO）合酶抑制剂NG-硝基-L-精氨酸对未麻醉、自由活动大鼠伏隔核中N-甲基-D-天冬氨酸（NMDA）诱导的多巴胺释放的影响。通过微透析探针灌注1 mM和3 mM的NMDA可剂量依赖性地增加伏隔核细胞外多巴胺水平。共同应用0.5 mM D-(-)-2-氨基-5-磷酸缬氨酸（D-AP5），一种选择性竞争性NMDA受体拮抗剂，可显著降低3 mM NMDA诱导的多巴胺释放。单独灌注0.5 mM NG-硝基-L-精氨酸不影响基础多巴胺水平，而当与3 mM NMDA同时应用时，它可抑制NMDA诱发的伏隔核多巴胺释放。这些结果表明，NO至少部分介导了大鼠伏隔核中NMDA受体激活导致的多巴胺释放。
