Hoppe D, Chvatal A, Kettenmann H, Orkand R K, Ransom B R
Department for Neurobiology, University of Heidelberg, F.R.G.
Brain Res. 1991 Jun 21;552(1):106-12. doi: 10.1016/0006-8993(91)90666-j.
Ion-sensitive microelectrodes were used to study the behavior of extracellular ions in rat sciatic nerve during and following activity. Nerve stimulation produced increases in [K+]o that were dependent upon the frequency and duration of stimulation; no change in extracellular pH occurred with stimulation. Increases in [K+]o depended on axonal discharge since they were blocked by inhibiting sodium channels with tetrodotoxin. At 22 degrees C, stimulation could induce increases in [K+]o of several mM; at 36 degrees C, stimulation rarely produced increases in [K+]o greater than 1 mM. Stimulated increases in [K+]o dissipated very slowly (i.e. t 1/2 = 50-100 s) and the rate of dissipation was not significantly affected by anoxia, changes in temperature, changes in extracellular pH, or the application of a blocker of Na+, K(+)-ATPase (ouabain) or a K+ channel blocker (Ba2+). In comparison to the central nervous system, neural activity in rat sciatic nerve produced smaller increases in [K+]o and these increases dissipated much more slowly. The primary mechanism of K+ dissipation appeared to be diffusion, probably facilitated by the larger extracellular space in peripheral nerve compared to the central nervous system, but impeded by diffusion barriers imposed by the blood-nerve barrier.
离子敏感微电极用于研究大鼠坐骨神经在活动期间及活动后的细胞外离子行为。神经刺激使细胞外[K+]升高，其依赖于刺激的频率和持续时间；刺激时细胞外pH无变化。细胞外[K+]升高依赖于轴突放电，因为用河豚毒素抑制钠通道可阻断这种升高。在22℃时，刺激可使细胞外[K+]升高数毫摩尔；在36℃时，刺激很少使细胞外[K+]升高超过1毫摩尔。刺激引起的细胞外[K+]升高消散非常缓慢（即半衰期=50-100秒），且消散速率不受缺氧、温度变化、细胞外pH变化或应用Na+，K(+)-ATP酶阻滞剂（哇巴因）或K+通道阻滞剂（Ba2+）的显著影响。与中枢神经系统相比，大鼠坐骨神经的神经活动使细胞外[K+]升高幅度较小，且这些升高消散得更慢。K+消散的主要机制似乎是扩散，可能是由于与中枢神经系统相比，外周神经细胞外间隙较大而促进扩散，但受血神经屏障施加的扩散屏障阻碍。
