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Shielding effects of myelin sheath on axolemma depolarization under transverse electric field stimulation

机译：髓鞘对横向电场刺激下轴突去极化的屏蔽作用

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Axonal stimulation with electric currents is an effective method for controlling neural activity. An electric field parallel to the axon is widely accepted as the predominant component in the activation of an axon. However, recent studies indicate that the transverse component to the axolemma is also effective in depolarizing the axon. To quantitatively investigate the amount of axolemma polarization induced by a transverse electric field, we computed the transmembrane potential (Vm) for a conductive body that represents an unmyelinated axon (or the bare axon between the myelin sheath in a myelinated axon). We also computed the transmembrane potential of the sheath-covered axonal segment in a myelinated axon. We then systematically analyzed the biophysical factors that affect axonal polarization under transverse electric stimulation for both the bare and sheath-covered axons. Geometrical patterns of polarization of both axon types were dependent on field properties (magnitude and field orientation to the axon). Polarization of both axons was also dependent on their axolemma radii and electrical conductivities. The myelin provided a significant “shielding effect” against the transverse electric fields, preventing excessive axolemma depolarization. Demyelination could allow for prominent axolemma depolarization in the transverse electric field, via a significant increase in myelin conductivity. This shifts the voltage drop of the myelin sheath to the axolemma. Pathological changes at a cellular level should be considered when electric fields are used for the treatment of demyelination diseases. The calculated term for membrane polarization (Vm) could be used to modify the current cable equation that describes axon excitation by an external electric field to account for the activating effects of both parallel and transverse fields surrounding the target axon.
机译：电流轴突刺激是控制神经活动的有效方法。平行于轴突的电场被广泛接受为激活轴突的主要成分。但是，最近的研究表明，轴突的横向分量在使轴突去极化方面也是有效的。为了定量研究横向电场引起的轴突极化量，我们计算了代表无髓鞘轴突（或有髓鞘轴突中髓鞘鞘之间的裸轴突）的导电体的跨膜电势（Vm）。我们还计算了髓鞘化轴突中鞘覆盖的轴突节的跨膜电位。然后，我们系统地分析了在裸露的和鞘覆盖的轴突的横向电刺激下影响轴突极化的生物物理因素。两种轴突类型的极化的几何图案都取决于场的性质（轴突的大小和场定向）。两个轴突的极化也取决于其轴突半径和电导率。髓磷脂对横向电场提供了显着的“屏蔽作用”，从而防止了过多的轴突去极化。脱髓鞘作用可以通过显着增加髓磷脂的电导率而在横向电场中引起明显的轴突去极化。这将髓鞘的电压降转移到腋窝。当使用电场治疗脱髓鞘疾病时，应考虑细胞水平的病理变化。膜极化（Vm）的计算项可用于修改当前电缆方程，该方程描述了外部电场对轴突的激发，以说明目标轴突周围平行和横向电场的激活作用。

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