Bostock H, Rasminsky M
J Physiol. 1983 Jul;340:145-56. doi: 10.1113/jphysiol.1983.sp014755.
We have used 4-aminopyridine (4AP), a potassium channel blocker, to assess the presence and distribution of potassium channels in the congenitally abnormally myelinated spinal root axons of dystrophic mice. 1 mM-4AP slightly depressed the amplitude but had no effect on the half-width of the monophasic action potential of normal A fibres, indicating the absence of a significant concentration of potassium channels at normal mouse nodes of Ranvier. By progressively increasing stimulus intensity it was possible to elicit three more or less discrete components of the compound action potential from dystrophic mouse spinal roots, presumably corresponding to myelinated fibres, large diameter bare axons and, in the case of dorsal roots, C fibres. The amplitude and duration of all three components were increased on exposure to 4AP, indicating the presence of potassium channels in all types of dystrophic mouse spinal root axons. Conduction in single fibres was studied using longitudinal current analysis. Both saltatory and continuous conduction were observed corresponding to the myelinated and bare portions of dystrophic mouse spinal root axons. Three types of 'nodal' membrane could be inferred from the membrane current recordings from myelinated dystrophic mouse axons: (1) pure sodium channel membrane, (2) membrane containing both sodium and potassium channels, and (3) membrane containing predominantly, if not exclusively, potassium channels. The large early outward currents at the latter two types of nodes suggested that these nodes were wider than normal. Recordings of continuous conduction indicated that potassium channels were also distributed irregularly along bare portions of the dystrophic mouse axons. These abnormalities of ion channel distribution are interpreted as reflecting failure of normal axon-Schwann cell communication in the dystrophic mouse spinal roots.
我们使用钾通道阻滞剂4-氨基吡啶（4AP）来评估营养不良小鼠先天性异常髓鞘化脊髓神经根轴突中钾通道的存在和分布。1 mM的4AP略微降低了正常A纤维单相动作电位的幅度，但对其半宽度没有影响，这表明在正常小鼠的郎飞结处不存在大量的钾通道。通过逐渐增加刺激强度，可以从营养不良小鼠的脊髓神经根中引出复合动作电位的三个或多或少离散的成分，推测分别对应有髓纤维、大直径无髓轴突，对于背根而言，还有C纤维。暴露于4AP后，所有三个成分的幅度和持续时间均增加，表明在所有类型的营养不良小鼠脊髓神经根轴突中均存在钾通道。使用纵向电流分析研究了单纤维的传导。观察到跳跃传导和连续传导，分别对应于营养不良小鼠脊髓神经根轴突的有髓部分和无髓部分。从营养不良小鼠有髓轴突的膜电流记录中可以推断出三种类型的“节点”膜：（1）纯钠通道膜，（2）同时含有钠通道和钾通道的膜，（3）主要（如果不是唯一）含有钾通道的膜。后两种类型节点处较大的早期外向电流表明这些节点比正常节点宽。连续传导的记录表明，钾通道也不规则地分布在营养不良小鼠轴突的无髓部分。这些离子通道分布异常被解释为反映了营养不良小鼠脊髓神经根中正常轴突-施万细胞通讯的失败。
