Resting membrane potential, the action potential and nerve conduction
How ion gradients and potassium permeability set the resting membrane potential, how voltage-gated channels generate and propagate the action potential, and how this explains the effects of potassium and calcium disorders, demyelination, local anaesthetics, sodium channel drugs and channelopathies.
Tier 1Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- The resting membrane potential (about −70 mV in neurons, −90 mV in skeletal and ventricular muscle) exists because the Na⁺/K⁺-ATPase keeps potassium high inside, and the resting membrane lets potassium leak out far more easily than sodium leaks in.
- An action potential is an all-or-none event: voltage-gated sodium channels open at threshold (about −55 mV), then inactivate within about 1 ms while potassium channels repolarise the cell.
- Conduction velocity rises with axon diameter and myelination. Myelinated axons conduct by saltatory conduction between nodes of Ranvier.
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Sources
- Principles of Neural Science (6th ed.)McGraw Hill (Kandel, Koester, Mack and Siegelbaum, 2021), 2021
- Guyton and Hall Textbook of Medical Physiology (14th ed.)Elsevier (Hall and Hall, 2021), 2021
- Australian Medicines HandbookAU/NZAustralian Medicines Handbook Pty Ltd, 2026
- Neal JM et al. The third American Society of Regional Anesthesia and Pain Medicine practice advisory on local anesthetic systemic toxicity: executive summary 2017. Reg Anesth Pain Med 2018;43:113-23Regional Anesthesia and Pain Medicine, 2018
- Last updated
- 14 November 2026
What changed
- 14 November 2026 Personal emails, About story and Australian-style copy