Lehmenkühler A
Institut für Physiologie der Universität Münster.
EEG EMG Z Elektroenzephalogr Elektromyogr Verwandte Geb. 1990 Mar;21(1):1-6.
Changes of brain cell microenvironment in the cerebral cortex of the rat were studied during spreading depression (SD) elicited by KCl application or local cooling. The question was whether the behavior of extracellular ion concentrations, especially of K+, could give some information about the triggering mechanisms of SD at the site where the phenomenon originates in the tissue. SDs elicited by KCl and recorded far from their original sites were associated with disturbances of extracellular ion concentrations and of tissue pO2 and pCO2 showing characteristic time sequences. Under these conditions none of the parameters studied changed before SD development. When an SD was elicited by local cooling extracellular K+ concentration ([K+]0) increased steeply in the mostly cooled cortical layers prior to SD initiation and formed a plateau of about 10 mmol/l resembling the ceiling level for K+ associated with ictal seizure activity. The front of the SD wave moved down slowly to the white matter. Thereby the rectangular rise in [K+]0 prior to SD progressively flattened and finally disappeared. The results suggest that SD evoked by local cooling originates from a primary increase of [K+]0 to the K+ ceiling level and by a secondary breakdown of the mechanisms being responsible for this type of K(+)-regulation. The mechanisms mentioned may be responsible for all kinds of SD-triggering.
在通过应用氯化钾或局部冷却引发的扩散性抑制（SD）过程中，对大鼠大脑皮层中脑细胞微环境的变化进行了研究。问题在于细胞外离子浓度，尤其是钾离子的浓度变化，是否能在该现象于组织中起源的部位提供有关SD触发机制的一些信息。由氯化钾引发并在远离其原始部位记录的SD与细胞外离子浓度以及组织pO₂和pCO₂的紊乱相关，呈现出特征性的时间序列。在这些条件下，所研究的参数在SD发展之前均未发生变化。当通过局部冷却引发SD时，在SD开始之前，大部分冷却的皮层层中细胞外钾离子浓度（[K⁺]₀）急剧增加，并形成了一个约10 mmol/L的平台，类似于与发作性癫痫活动相关的钾离子上限水平。SD波的前沿缓慢向下移动至白质。由此，SD之前[K⁺]₀的矩形升高逐渐变平并最终消失。结果表明，局部冷却引发的SD起源于[K⁺]₀的原发性增加至钾离子上限水平，以及负责这种类型钾离子调节的机制的继发性破坏。上述机制可能是所有类型SD触发的原因。
