Butcher S P, Lazarewicz J W, Hamberger A
Institute of Neurobiology, University of Göteborg, Sweden.
J Neurochem. 1987 Nov;49(5):1355-60. doi: 10.1111/j.1471-4159.1987.tb00999.x.
The in vivo effects of kainate (1 mM) on fluxes of 45Ca2+, and endogenous amino acids, were examined in the rat striatum using the brain microdialysis technique. Kainate evoked a rapid decrease in dialysate 45Ca2+, and an increase in the concentration of amino acids in dialysates in Ca2+-free dialysates. Taurine was elevated six- to 10-fold, glutamate two- to threefold, and aspartate 1.5- to twofold. There was also a delayed increase in phosphoethanolamine, whereas nonneuroactive amino acids were increased only slightly. The kainic acid-evoked reduction in dialysate 45Ca2+ activity was attenuated in striata lesioned previously with kainate, suggesting the involvement of intrinsic striatal neurons in this response. The increase in taurine concentration induced by kainate was slightly smaller under these conditions. Decortication did not affect the kainate-evoked alterations in either dialysate 45Ca2+ or amino acids. These data suggest that kainate does not release acidic amino acids from their transmitter pools located in corticostriatal terminals.
采用脑微透析技术,在大鼠纹状体中研究了海人酸(1 mM)对45Ca2+通量以及内源性氨基酸的体内效应。在无钙透析液中,海人酸引起透析液中45Ca2+迅速减少,氨基酸浓度增加。牛磺酸升高了6至10倍,谷氨酸升高了2至3倍,天冬氨酸升高了1.5至2倍。磷酸乙醇胺也有延迟增加,而非神经活性氨基酸仅略有增加。预先用海人酸损伤的纹状体中,海人酸引起的透析液45Ca2+活性降低减弱,提示内源性纹状体神经元参与了这一反应。在这些条件下,海人酸诱导的牛磺酸浓度增加略小。去皮质术不影响海人酸引起的透析液45Ca2+或氨基酸的变化。这些数据表明,海人酸不会从位于皮质纹状体终末的递质池中释放酸性氨基酸。