Gordon T R, Kocsis J D, Waxman S G
Department of Neurology, Yale University School of Medicine, West Haven, CT 06516.
Neuroscience. 1990;37(3):829-37. doi: 10.1016/0306-4522(90)90112-h.
Rat optic nerves were studied in a sucrose gap chamber in order to study the origin of a late afterhyperpolarization that follows repetitive activity. The results provide evidence for electrogenic pump (Na+/K(+)-ATPase) activity in central nervous system myelinated axons and demonstrate an effect on axonal excitability. Repetitive stimulation (25-200 Hz; 200-5000 ms) led to a prolonged, temperature-dependent post-train afterhyperpolarization with duration up to about 40 s. The post-train afterhyperpolarization was blocked by the Na+/K(+)-ATPase blockers strophanthidin and ouabain, and the substitution of Li+ for Na+ in the test solution, which also blocks Na+/K(+)-ATPase. The peak amplitude of the post-train afterhyperpolarization was minimally changed by the potassium-channel blocker tetraethylammonium (10 mM), and the Ca2(+)-channel blocker CoCl2 (4 mM). Hyperpolarizing constant current did not reverse the afterhyperpolarization. The amplitude of the hyperpolarization was increased in the presence of the potassium-channel blocker 4-aminopyridine (1 mM). In the presence of 4-amino-pyridine, the post-train hyperpolarization was much reduced by strophanthidin, except for a residual early component lasting several hundred milliseconds which was blocked by the potassium-channel blocker tetraethylammonium. This finding indicates that after exposure to 4-aminopyridine, repetitive stimulation leads to activation of a tetraethylammonium-sensitive K(+)-channel that contributes during the first several hundred milliseconds to the post-train afterhyperpolarization. The amplitude of the compound action potential elicited by a single submaximal stimulus during the post-train hyperpolarization was smaller than that of the control response. The decrement in amplitude was not present under identical stimulation conditions when the post-train hyperpolarization was blocked by strophanthidin, indicating that the hyperpolarization associated with repetitive stimulation reduced excitability.(ABSTRACT TRUNCATED AT 250 WORDS)
为了研究重复活动后出现的延迟超极化的起源，在蔗糖间隙室中对大鼠视神经进行了研究。结果为中枢神经系统有髓轴突中的电生泵（Na+/K(+)-ATP酶）活性提供了证据，并证明了其对轴突兴奋性的影响。重复刺激（25 - 200 Hz；200 - 5000 ms）导致了一种持续时间长达约40秒的、与温度相关的训练后延迟超极化。训练后延迟超极化被Na+/K(+)-ATP酶阻滞剂毒毛花苷和哇巴因阻断，以及在测试溶液中用Li+替代Na+（这也会阻断Na+/K(+)-ATP酶）。训练后延迟超极化的峰值幅度受钾通道阻滞剂四乙铵（10 mM）和钙通道阻滞剂CoCl2（4 mM）的影响最小。超极化恒流并未使延迟超极化反转。在存在钾通道阻滞剂4 - 氨基吡啶（1 mM）的情况下，超极化幅度增加。在存在4 - 氨基吡啶的情况下，训练后超极化被毒毛花苷大大降低，除了持续数百毫秒的残余早期成分，该成分被钾通道阻滞剂四乙铵阻断。这一发现表明，在暴露于4 - 氨基吡啶后，重复刺激会导致一种对四乙铵敏感的钾通道激活，该通道在最初几百毫秒内对训练后延迟超极化有贡献。在训练后超极化期间，由单个次最大刺激引发的复合动作电位的幅度小于对照反应。当训练后超极化被毒毛花苷阻断时，在相同刺激条件下幅度减小现象不存在，这表明与重复刺激相关的超极化降低了兴奋性。（摘要截短于250字）
