查看Ch12 Physiology of Neurons的源代码

=== 脱髓鞘轴突缓慢、不可靠或根本不传导动作电位 ===
<b style=color:#0ae>Demyelinated axons conduct action potentials slowly, unreliably, or not at all</b>

Numerous clinical disorders selectively damage or destroy myelin sheaths and leave the axonal membranes intact but bare. These demyelinating diseases may affect either peripheral or central axons and can lead to severely impaired conduction (Fig. 12-6). The most common demyelinating disease of the CNS is multiple sclerosis (Box 12-1), a progressive disorder characterized by distributed zones of demyelination in the brain and spinal cord. The specific clinical signs of these disorders vary and depend on the particular sets of axons affected.

许多临床疾病选择性地损伤或破坏髓鞘，使轴突膜完好无损但裸露。这些脱髓鞘疾病可能影响外周或中央轴突，并可能导致严重的传导受损（图 12-6）。CNS 最常见的脱髓鞘疾病是多发性硬化症 （Box 12-1），这是一种进行性疾病，其特征是大脑和脊髓中分布的脱髓鞘区。这些疾病的具体临床症状各不相同，取决于受影响的特定轴突集。


In a normal, myelinated axon, the action currents generated at a node can effectively charge the adjacent node and bring it to threshold within ~20 μsec (Fig. 12-7A), because myelin serves to increase the resistance and to reduce the capacitance of the pathways between the axoplasm and the extracellular fluid (see pp. 199–201). The inward membrane current flowing across each node is actually 5-fold to 7-fold higher than necessary to initiate an action potential at the adjacent node. Removal of the insulating myelin, however, means that the same nodal action current is distributed across a much longer, leakier, higher-capacitance stretch of axonal membrane (see Fig. 12-7B). Several consequences are possible. Compared with normal conduction, conduction in a demyelinated axon may continue, but at a lower velocity, if the demyelination is not too severe (see Fig. 12-7B, record 1). In experimental studies, the internodal conduction time through demyelinated fibers can be as slow as 500 μs, 25 times longer than normal. The ability of axons to transmit high-frequency trains of impulses may also be impaired (see Fig. 12-7B, record 2). Extensive demyelination of an axon causes total blockade of conduction (see Fig. 12-7B, record 3). Clinical studies indicate that the blockade of action potentials is more closely related to symptoms than is the simple slowing of conduction. Demyelinated axons can also become the source of spontaneous, ectopically generated action potentials because of changes in their intrinsic excitability (see Fig. 12-7B, record 4) or mechanosensitivity (see Fig. 12-7B, record 5). Moreover, the signal from one demyelinated axon can excite an adjacent demyelinated axon and induce crosstalk (see Fig. 12-7C), which may cause action potentials to be conducted in both directions in the adjacent axon.

在正常的有髓轴突中，节点处产生的动作电流可以有效地为相邻节点充电，并在 ~20 μsec 内使其达到阈值（图 12-7A），因为髓鞘的作用是增加电阻并降低轴质和细胞外液之间通路的电容（见第 199-201 页）。流过每个节点的向内膜电流实际上比在相邻节点启动动作电位所需的电流高 5 到 7 倍。然而，去除绝缘髓鞘意味着相同的节点作用电流分布在更长、泄漏更大、电容更高的轴突膜上（见图 12-7B）。可能有多种后果。与正常传导相比，如果脱髓鞘不太严重，脱髓鞘轴突中的传导可能会继续，但速度会更低（见图 12-7B，记录 1）。在实验研究中，通过脱髓鞘纤维的结间传导时间可慢至 500 μs，比正常时间长 25 倍。轴突传递高频脉冲序列的能力也可能受损（见图 12-7B，记录 2）。轴突的广泛脱髓鞘导致传导完全阻塞（参见图 12-7B，记录 3）。临床研究表明，动作电位的阻断与症状的相关性比简单的传导减慢更密切。脱髓鞘的轴突也可以成为自发的、异位产生的动作电位的来源，因为它们的内在兴奋性（见图 12-7B，记录 4）或机械敏感性（见图 12-7B，记录 5）发生了变化。此外，来自一个脱髓鞘轴突的信号可以激发相邻的脱髓鞘轴突并诱导串扰（见图 12-7C），这可能导致动作电位在相邻轴突中双向传导。

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