Lux H D
Arch Psychiatr Nervenkr (1970). 1976 Apr 30;221(3):227-44. doi: 10.1007/BF00418482.
Two mechanisms are discussed which link extracellular potassium accumulation and epileptogenic neuronal hyperactivity in the cortex. The potassium concentration (aK) of the environment of a repetitively discharging membrane can increase sufficiently for a supra-threshold depolarization at afferent erminals. This can explain the finding of ectopic spike generation and the antidromic breakthrough in thalamo-cortical projections after a primary cortical discharge. Spread and recurrent enhancement of excitatory drives may be the result of this mechanism. Initiation and termination of seizure is not explained by potassium accumulation. There is a ceiling level in potassium of about 10 mequ/1 which is strictly maintained during normal as well as epileptiform activity. This level is probably not high enough for depolarizing inactivation of neuronal membranes. Stimulation of cortical afferents can have a dual effect on aK. After a primary shortlasting increase, aK can reach subnormal values. This is possibly brought about by a stimulated re-uptake of K+. Seizures can be initiated at these subnormal levels. The effect of the re-uptake e.g. hyperpolarization of terminal afferents and increase of evoked transmitter release is discussed for the initiation for paroxysmal activity.
本文讨论了两种将细胞外钾离子蓄积与皮层癫痫源性神经元活动亢进联系起来的机制。重复放电膜周围环境中的钾离子浓度（aK）可充分升高，足以使传入终末发生阈上 depolarization。这可以解释在原发性皮层放电后，异位 spike 产生以及丘脑 - 皮层投射中的逆向突破现象。兴奋性驱动的扩散和反复增强可能是这种机制的结果。癫痫发作的起始和终止不能用钾离子蓄积来解释。钾离子存在一个约 10 毫当量/升的上限水平，在正常及癫痫样活动期间严格维持。该水平可能不足以使神经元膜发生去极化失活。刺激皮层传入神经对 aK 可产生双重作用。在最初短暂升高后，aK 可降至低于正常的值。这可能是由刺激的钾离子再摄取引起的。在这些低于正常的水平下可引发癫痫发作。本文讨论了再摄取的作用，例如终末传入神经的 hyperpolarization 和诱发递质释放增加对阵发性活动起始的影响。
