Yamamoto B K, Davy S
Department of Psychiatry, Case Western Reserve University School of Medicine, Cleveland, OH 44106.
J Neurochem. 1992 May;58(5):1736-42. doi: 10.1111/j.1471-4159.1992.tb10048.x.
Glutamate and aspartate are the primary neurotransmitters of projections from motor and premotor cortices to the striatum. Release of glutamate may be modulated by dopamine receptors located on corticostriatal terminals. The present study used microdialysis to investigate the dopaminergic modulation of in vivo striatal glutamate and aspartate release in the striatum of awake-behaving rats. Local perfusion with a depolarizing concentration of K+ through a dialysis probe into the rat striatum produced a significant increase in the release of glutamate, aspartate, and taurine. The D2 agonist LY171555 blocked the K(+)-induced release of glutamate and aspartate, but not taurine, in a concentration-dependent manner. The D1 agonist SKF 38393 did not alter K(+)-induced release of glutamate and taurine, but did significantly decrease aspartate release. Neither agonist had any effect on basal amino acid release. The D2 antagonist (-)-sulpiride reversed the inhibitory effects of LY 171555 on K(+)-induced glutamate release. These results provide in vivo evidence for a functional interaction between dopamine, the D2 receptor, and striatal glutamate release.
谷氨酸和天冬氨酸是从运动皮质和运动前皮质投射到纹状体的主要神经递质。谷氨酸的释放可能受位于皮质纹状体终末的多巴胺受体调节。本研究采用微透析技术，以探究清醒行为大鼠纹状体内多巴胺能对体内纹状体谷氨酸和天冬氨酸释放的调节作用。通过透析探针向大鼠纹状体内局部灌注去极化浓度的钾离子，可使谷氨酸、天冬氨酸和牛磺酸的释放显著增加。D2激动剂LY171555以浓度依赖性方式阻断钾离子诱导的谷氨酸和天冬氨酸释放，但不影响牛磺酸释放。D1激动剂SKF 38393不改变钾离子诱导的谷氨酸和牛磺酸释放，但显著降低天冬氨酸释放。两种激动剂对基础氨基酸释放均无影响。D2拮抗剂（-）-舒必利可逆转LY 171555对钾离子诱导的谷氨酸释放的抑制作用。这些结果为多巴胺、D2受体与纹状体谷氨酸释放之间的功能相互作用提供了体内证据。
