Heinemann U, Dietzel I
J Neurophysiol. 1984 Sep;52(3):421-34. doi: 10.1152/jn.1984.52.3.421.
Changes in extracellular K+ concentration [( K+]o) were measured with ion-selective microelectrodes in chronic epileptic foci induced by topical application of A1(OH)3 cream on the sensorimotor cortex of cats. The foci were morphologically characterized by a scar surrounded by an area of marked gliosis. Base-line levels of [K+]o in gliotic tissue and its immediate border zone were comparable to those in normal cortical tissue. Peak levels of [K+]o obtained during repetitive electrical stimulation of the cortical surface and thalamic ventrobasal complex were only slightly enhanced with 11.6 mM in chronic foci and 10.8 mM in normal cortex. Iontophoretic K+ application into gliotic tissue was accompanied by slow negative potential shifts comparable to those observed in normal cortex. Passage of constant current through gliotic tissue caused local [K+]o changes in the vicinity of the current-passing electrode. Since these [K+]o changes were similar to those observed in normal tissue, it was concluded that the amount of transcellularly transported K ions was comparable in both tissues. Changes in the size of extracellular space (ES) were investigated by measuring local concentration changes of iontophoretically injected tetramethylammonium and choline ions. During stimulus-induced seizure activity, the ES shrank outside the gliotic area at sites of maximal [K+]o elevation, while it increased at sites within the gliotic tissue where [K+]o rises were smaller. The results suggest that the spatial buffer capacity of gliotic tissue for K+ is not severely impaired. Since the relationship between rises in [K+]o and subsequent undershoots at sites immediately bordering the gliotic tissue is comparable to that in normal cortex, the ability of this epileptic tissue for active K+ uptake appears to be unaffected. This conclusion is further supported by the observation that iontophoretically induced rises in [K+]o during undershoots are reduced to a similar extent as in normal cortex.
通过离子选择性微电极测量了在猫的感觉运动皮层局部应用氢氧化铝乳膏诱导的慢性癫痫病灶中细胞外钾离子浓度[K⁺]ₒ的变化。这些病灶在形态学上的特征是有一个瘢痕，周围是明显的胶质增生区域。胶质增生组织及其紧邻边界区域的[K⁺]ₒ基线水平与正常皮质组织相当。在重复电刺激皮质表面和丘脑腹侧基底复合体期间获得的[K⁺]ₒ峰值水平，在慢性病灶中仅略有升高至11.6 mM，在正常皮质中为10.8 mM。向胶质增生组织中离子导入钾离子伴随着缓慢的负电位变化，与在正常皮质中观察到的相似。恒定电流通过胶质增生组织会导致在通电电极附近局部[K⁺]ₒ发生变化。由于这些[K⁺]ₒ变化与在正常组织中观察到的相似，因此得出结论，两个组织中跨细胞转运的钾离子量相当。通过测量离子导入注入的四甲基铵和胆碱离子的局部浓度变化来研究细胞外空间（ES）大小的变化。在刺激诱发的癫痫发作活动期间，在[K⁺]ₒ升高最大的部位，胶质增生区域外的ES缩小，而在[K⁺]ₒ升高较小的胶质增生组织内的部位，ES增大。结果表明，胶质增生组织对钾离子的空间缓冲能力没有严重受损。由于在紧邻胶质增生组织的部位，[K⁺]ₒ升高与随后的负电位变化之间的关系与正常皮质中的相当，因此这种癫痫组织主动摄取钾离子的能力似乎未受影响。离子导入诱发的负电位期间[K⁺]ₒ升高与正常皮质中降低程度相似的观察结果进一步支持了这一结论。
