Young A M, Crowder J M, Bradford H F
Department of Biochemistry, Imperial College of Science and Technology, London, England.
J Neurochem. 1988 Feb;50(2):337-45. doi: 10.1111/j.1471-4159.1988.tb02918.x.
The effect of kainate on extracellular levels of amino acids in corpus striatum was investigated in vitro and in vivo, to elucidate the mechanism underlying its neurotoxicity. Kainate increased extracellular glutamate and aspartate in both striatal slices in vitro and intact striatum in vivo, as previously reported. Both in vitro and in vivo, DL-threo-3-hydroxyaspartate increased extracellular glutamate and aspartate levels (to between 150 and 200% of basal), and also enhanced their kainate-evoked release. The action of kainate in vivo was reduced by prior frontal decortication, whereas in vitro the kainate-evoked responses were only slightly reduced by tetrodotoxin, and remained above control values. These results confirm that kainate increases extracellular glutamate and aspartate, and provide evidence that this is due to synaptic release evoked by an action on receptors on glutamatergic neurone terminals. These findings may be relevant to the understanding of epilepsy.
为阐明红藻氨酸神经毒性的潜在机制，我们在体外和体内研究了红藻氨酸对纹状体中细胞外氨基酸水平的影响。如先前报道，红藻氨酸在体外增加了纹状体切片中的细胞外谷氨酸和天冬氨酸水平，在体内增加了完整纹状体中的细胞外谷氨酸和天冬氨酸水平。在体外和体内，DL-苏式-3-羟基天冬氨酸均增加了细胞外谷氨酸和天冬氨酸水平（至基础水平的150%至200%之间），并增强了它们由红藻氨酸诱发的释放。预先进行额叶皮质切除术可降低红藻氨酸在体内的作用，而在体外，河豚毒素仅轻微降低红藻氨酸诱发的反应，且反应仍高于对照值。这些结果证实红藻氨酸增加了细胞外谷氨酸和天冬氨酸，并提供证据表明这是由于对谷氨酸能神经元终末受体的作用诱发的突触释放所致。这些发现可能与癫痫的理解有关。
