Release of amino acids from chronic epileptic and sub-epileptic foci in vivo
Release of amino acids from chronic epileptic and sub-epileptic foci in vivo
复制标题
体内慢性癫痫病灶和亚癫痫病灶中氨基酸的释放
DOI：
10.1016/0006-8993(80)90180-8
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发表时间：
1980
期刊：
影响因子：
2.9
通讯作者：
J. Continho
中科院分区：
文献类型：
--
作者：
P. Dodd;H. Bradford;A. Abdul;D. Cox;J. Continho
在大鼠大脑皮层感觉运动带内植入穿孔的钴或镍盘。Co椎间盘引起对侧肌阵挛性肢体抽搐，其方式与Co粉病变相似。相比之下，植入镍的动物从未观察到明显的肢体抽搐。在体内插管系统的灌注下，与未损伤组织相比，两种类型的病变释放的谷氨酸、缬氨酸和甘氨酸的量都增加。然而，与非癫痫性病变相比，致痫性病变的Co释放增强约为3倍。此外，与对照组相比，癫痫性病变显示谷氨酰胺释放明显减少，而非癫痫性病变则没有。讨论了谷氨酸/谷氨酰胺系统的局部紊乱可能参与钴灶多动的产生。
Perforated discs of cobalt or nickel were implanted onto the sensorimotor strip of the cerebral cortex of rats. Co discs gave rise to myoclonic contralateral limb-jerks in a manner similar to Co powder lesions. In contrast, Ni-implanted animals were never observed to show overt limb-jerks. On superfusion with an in vivo cannula system, both types of lesion released increased amounts of glutamate, valine and glycine as compared with unlesioned tissue. However, the enhancement of release from epileptogenic Co lesions was approximately 3-fold greater than that from non-epileptogenic lesions. In addition, epileptogenic lesions showed a marked reduction in glutamine release compared to controls, while non-epileptogenic lesions did not. The possible involvement of local disorders of the glutamate/glutamine system in the generation of cobalt focus hyperactivity is discussed.