Question

Explain the impact that changes in sodium (Na), potassium (K), or even myelination will have on nerve conduction.

Answer 1

Electrical axonal propagation of the action potential (AP) is required for function such as motor output; control of visceral organs tec. Initiation of the AP occurs at the axon initial segment (AIS) rich in voltage-gated ion channels, particularly voltage-gated sodium channels (Nav). Entry of sodium through these channels causes membrane depolarization that is passed to the next segment of neuronal membrane. Efflux of potassium ions (Kv) in regions trailing the action potential will inactivate Nav due to hyperpolarization. Thus, the axonal membrane patches returns back to its resting potential.

The Na+-K+ ATpase pump will transport three sodium ions into the cell and two potassium ions outside the cell. When extracellular sodium increases, the membrane is depolarized due to entry of sodium inside the membrane. This depolarization spreads to adjacent distal regions, thereby opening few more Nav. As more Na+ ions enter the cell, there is more depolarization. This will increase neuronal conduction. When there is less extracellular sodium, there will be more hyperpolarization causing a decrease in membrane conductance. Sodium channels are inhibited by toxins such as teradotoxin (TTX). TTX binds to subunits of sodium channels and inactivate them. Thus, sodium movement is inhibited. Hence, nerve conductance is decreased slowly. Thus, depolarization will increase nerve conduction velocity while hyperpolarization will reduce nerve conductance.

Extracellular K+ increase will not affect initial conductance velocity. They will infact increase nerve conductance. However, larger deviation in extracellular potassium will slow nerve conductance. When there is low extracellular K+, there will be accumulated of intracellular Na+ with each action potential. As there is low K+, there will be some outward movement of K+. However, due to limited intracellular volume of the unmyelinated axons, the flow of K+ outside the cell will cause depolarization of axons. When extracellular K+ ion increases, there will be more hyperpolarization seen. Thus, there will be less conduction velocity seen.

Myelin sheath is a sack of plasma membrane sheet that is produced by a glial cell. Myelin is wrapped around the axon of a nerve. This myelin membrane has phospholipids but has relatively less proteins. Node of Ranvier is an unmeylinated area that separates tow myelinated axons. Myelin prevents transfer of ions between the axonal cytosol and the extracellular fluid. Hence, electrical activity is limited to nodes of Ranvier where ions are transferred from the axonal cytosol with the extracellular fluid. Glial cells secrete proteins that stimulate voltage gated Na+ channels at the nodes. Hence, nodes have more Na+ gated channels than the myelinated axons. Hence, excess sodium ions generated by depolarization associated with action potential will pass passively through axonal cytosol to the next node without any attenuation. As a result, action potential will increase from node to node. Thus, conduction velocity of myelinated fibers is higher than non myelinated fibers of same length. It takes only 0.01 sec for an action potential to travel the length of the axon to stimulate action potential.