Grisar T
Ann Neurol. 1984;16 Suppl:S128-34. doi: 10.1002/ana.410160719.
Because high extracellular K+ concentrations (18-20 mM) increased glial Na+- and K+ -dependent adenosine triphosphatase [(Na+ + K+)-ATPase] activities, while this increase was not observed in neuronal preparations, it is hypothesized that K+ released in the extracellular space during neuronal firing is actively taken up by glial cells. In acute and chronic epileptogenic lesions of cats, glial (Na+ + K+)-ATPase dramatically decreased when compared to both control animals and the perifocal area, while its activation by extracellular K+ in concentrations between 3 and 18 mM was absent 3, 6, and up to 45 days after production of freezing lesions. Similar results were observed in 13 specimens of anterolateral temporal neocortex obtained during temporal lobectomies in patients with intractable temporal lobe epilepsy, compared with postmortem human specimen or control brain tissues. Hence, a glial (Na+ + K+)-ATPase abnormality exists in epileptogenic tissue. Further experimental data are presented supporting the notion that this glial abnormality may favor the transition from interictal episodes to ictal phenomena.
由于细胞外高钾浓度（18 - 20 mM）会增加胶质细胞钠钾依赖型三磷酸腺苷酶[（Na⁺ + K⁺）-ATP酶]的活性，而在神经元标本中未观察到这种增加，因此推测神经元放电期间释放到细胞外空间的钾离子会被胶质细胞主动摄取。在猫的急性和慢性致痫性病变中，与对照动物和病灶周围区域相比，胶质细胞（Na⁺ + K⁺）-ATP酶显著降低，而在冷冻损伤产生后3天、6天直至45天，其对3至18 mM细胞外钾离子的激活作用消失。在难治性颞叶癫痫患者颞叶切除术中获取的13个前外侧颞叶新皮质标本中，与死后人体标本或对照脑组织相比，也观察到了类似结果。因此，致痫组织中存在胶质细胞（Na⁺ + K⁺）-ATP酶异常。本文还提供了进一步的实验数据，支持这种胶质细胞异常可能有利于从发作间期向发作期现象转变这一观点。
