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▲ FIGURE 7-40 Conduction of action potentials in myelinated axons. Because voltage-gated Na+ channels are localized to the axonal membrane at the nodes of Ranvier, the influx of Na+ ions associated with an action potential can occur only at nodes. When an action potential is generated at one node (step 1), the excess positive ions in the cytosol, which cannot move outward across the sheath, diffuse rapidly down the axon, causing sufficient depolarization at the next node (step 2|) to induce an action potential at that node (step 3). By this mechanism the action potential jumps from node to node along the axon.

Ranvier. Both of these transport proteins interact with two cytoskeletal proteins, ankyrin and spectrin, similar to those in the erythrocyte membrane (see Figure 5-31). The extracellular domain of the subunit of the Na+ channel also binds to the extracellular domain of Nr-CAM, a type of adhesive protein that is localized to the node. As a result of these multiple protein-protein interactions, the concentration of Na+ channels is roughly a hundredfold higher in the nodal membrane of myelinated axons than in the axonal membrane of nonmyelinated neurons. In addition, glial cells secrete protein hormones that somehow trigger the clustering of these nerve membrane proteins at the nodes. Finally, tight junctions between the axon and the glial cell plasma membrane in the paranodal junctions immediately adjacent to the nodes may prevent diffusion of Na+ channels and Na+/K+ pumps away from the nodes.

One prevalent neurological disease among human adults is multiple sclerosis (MS), usually characterized by spasms and weakness in one or more limbs, bladder dysfunction, local sensory losses, and visual disturbances. This disorder—the prototype demyelinating disease—is caused by patchy loss of myelin in areas of the brain and spinal cord. In MS patients, conduction of action potentials by the demyelinated neurons is slowed, and the

Na+ channels spread outward from the nodes, lowering their nodal concentration. The cause of the disease is not known but appears to involve either the body's production of auto-antibodies (antibodies that bind to normal body proteins) that react with myelin basic protein or the secretion of proteases that destroy myelin proteins. I

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