Recent insights into axonal physiology and its measurement

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• 作者：D. Burke
• 刊名：Clinical Neurophysiology
• 出版年：2016
• 出版时间：March 2016
• 年：2016
• 卷：127
• 期：3
• 页码：e27
• 全文大小：37 K

文摘

Disturbances of axonal excitability determine many symptoms in patients. There are now rapid and reliable physiologic tests, using “threshold tracking”, that can be used in vivo to study axonal excitability. In humans, sensory and motor axons differ in two conductances, with consequent implications for the susceptibility toconduction block [motor axons] and to ectopic activity [sensory axons]:

The Na_v1.6 Na⁺ channel at the healthy mature node of Ranvier can have two gating modes: transient (∼98–99% total Na⁺ conductance) and persistent (∼1–2% total Na⁺ conductance). The persistent current is greater in sensory axons than motor. The persistent current is the reason for the difference in strength-duration properties, ∣_SD and rheobase. Most of this is because sensory axons are ∼4 mV more depolarized.

The hyperpolarisation-activated current (I_h) is internodally located, passes a depolarizing current, dependent on HCN channels. I_h contributes to resting membrane potential, and is more active on sensory axons than motor [and more on motor axons of low threshold]. The roleof I_h is to limit the neuronal/axonal hyperpolarisation, during, e.g., activity.

The excitability of peripheral nerve axons can be altered in central diseases, and this will be illustrated for K⁺ channel mutations underlying EA1 and BFNE.