Expression of the apamin-sensitive K+ channel (SK+) in rat skeletal muscle is neurally regulated. The regulatory effect of the nerve over the expression of some muscle ion channels has been attributed to the electrical activity triggered by the nerve and/or to a trophic effect of some molecules transported from the soma to the axonal endings. 2. SK+ channels apparently are involved in myotonic dystrophy (MD), therefore understanding the factors that regulate their expression may ultimately have important clinical relevance. 3. To establish if axoplasmic transport is involved in this process, we used two experimental approaches in adult rats: (a) Both sciatic nerves were severed, leaving a short or a long nerve stump attached to the anterior tibialis (AT). (b) Colchicine or vinblastine (VBL), two axonal transport blockers of different potencies, was applied on one leg to the sciatic nerve. To determine whether electrical activity affects the expression of SK+ channels, denervated AT were directly stimulated. The corresponding contralateral muscles were used as controls.
摘要
大鼠骨骼肌中蜂毒明肽敏感钾通道（SK +）的表达受神经调节。神经对某些肌肉离子通道表达的调节作用归因于神经触发的电活动和/或从胞体运输到轴突末梢的某些分子的营养作用。2. SK +通道显然与强直性肌营养不良（MD）有关，因此了解调节其表达的因素最终可能具有重要的临床意义。3. 为了确定轴浆运输是否参与此过程，我们在成年大鼠中采用了两种实验方法：（a）切断双侧坐骨神经，使胫前肌（AT）附着短或长的神经残端。（b）将秋水仙碱或长春碱（VBL）这两种不同效力的轴突运输阻滞剂应用于一侧腿部的坐骨神经。为了确定电活动是否影响SK +通道的表达，对去神经支配的AT进行直接刺激。相应的对侧肌肉用作对照。
