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Nerve action potential termination mechanism

Sodium and Potassium in the resting cell:The resting cell has an electrical potential-resting membrane potential- approximately -60 to -70mV in neurons (0 is convention for extracellular potential). Neurons at rest are more permeable to K+ ions than Na+ ions because of K+ leak channels; thus, membrane potential is closer to equilibrium potential of K+ (Ek+ -80 mV, eNa+ +60mV).

Action Potentials and their termination:Action potentials are brief, localized spikes of ( + ) charge on the cell membrane caused by rapid influx of Na+ ions along the electrochemical gradient (as above), peaking around +50mV. The rising phase slows and comes to a halt as the sodium ion channels become maximally open. The same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores, thereby making them inactivated. This lowers the membrane’s permeability to sodium relative to potassium, driving the membrane voltage back towards the resting potential. Concomitantly, the raised voltage opens voltage-sensitive potassium channels. Together, these changes in sodium and potassium permeability cause the membrane potential to drop quickly, repolarizing the membrane and producing the falling phase of the action potential.

The passive diffusion of membrane depolarization triggers other action potentials in either adjacent cell membrane in nonmyelinated nerve fibers or adjacent nodes of Ranvier in myelinated nerve fibers, resulting in a wave of action potential being propagated along the nerve. If the action potential is not regenerated along the neuron, passive decay of the potential occurs with distance, based on the model of decremental conduction, and the trigger threshold for the all-or-none phenomenon of action potential generation is not reached.

The role of Local Anesthetics in Action Potential Termination:If the nodes downstream of an AP are occupied by a concentration of (local anesthetic) LA high enough to block 74-84% of the sodium conductance, then the action potential amplitudes decrease at successive nodes. Eventually, the impulse decays to below-threshold amplitude if the series of LA containing nodes is long enough. Propagation of the impulse is then blocked by decremental conduction, even though none of the nodes are completely blocked. Concentrations of LA that block more than 84% of the sodium conductance at 3 successive nodes prevent any impulse propagation at all. (From Fink BR: Mechanism of differential axial blockade in epidural and spinal anesthesia ANS 1989.)


  1. A L HODGKIN, A F HUXLEY A quantitative description of membrane current and its application to conduction and excitation in nerve. J. Physiol. (Lond.): 1952, 117(4);500-44 PubMed Link
  2. Fink BR: Mechanisms of differential axial blockade in epidural and spinal anesthesia. Anesthesiology 1989 May;70(5):851-8. PubMed Link