Dimitrov Alexander G
Centre of Biomedical Engineering, Bulgarian Academy of Sciences, Sofia, Bulgaria.
Pflugers Arch. 2009 Jul;458(3):547-61. doi: 10.1007/s00424-009-0640-8. Epub 2009 Feb 10.
A unique mechanism is proposed according to which processes within the internodal axolemma are responsible for repetitive activation of myelinated axon with deficit of internodal potassium conductance. A numerical simulation of activity in axon with 21 nodes was performed. The axon was represented by cables for axoplasmic and periaxonal spaces. Accumulation and diffusion of ions were taken into account. Fine segmentation of each internode (338 segments) allowed simulation of internodal activation in response to a normal saltatorial action potential initiated by a short stimulus. The internodal membrane without potassium conductance experienced considerable depolarization. This resulted in formation of a transition zone and significant currents that caused repetitive activation of the internode and neighbor node. Decline of periaxonal sodium concentration during the spike production or lowering of sodium channel density decreased the sodium currents. As a result, the interspike intervals increased up to cessation of the burst. The cessation was reversible.
提出了一种独特的机制，根据该机制，节间轴膜内的过程负责节间钾电导不足的有髓轴突的重复激活。对具有21个节点的轴突活动进行了数值模拟。轴突由轴浆和轴周空间的电缆表示。考虑了离子的积累和扩散。每个节间的精细分割（338个片段）允许模拟节间对由短刺激引发的正常跳跃动作电位的激活。没有钾电导的节间膜经历了相当大的去极化。这导致形成一个过渡区和显著的电流，从而引起节间和相邻节点的重复激活。在产生尖峰期间轴周钠浓度的下降或钠通道密度的降低会降低钠电流。结果，峰间间隔增加直至爆发停止。这种停止是可逆的。
