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How nerve signals travel

An action potential swings the inside of a neuron from -70 mV to +30 mV and back in about 2 milliseconds.

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Set the stimulus and press Stimulate. Below +15 mV the trigger zone only wobbles; at +15 mV or more it fires. Turn Myelin off to compare the two ways a signal moves along the axon. Speeds are slowed and not to scale.

A tiny battery across the membrane

Every neuron keeps a small electrical difference across its membrane. It is measured on the inside compared with the outside, in millivolts (mV). At rest the inside sits at about -70 mV. Two things set this up. Sodium ions (Na+) are about ten times more concentrated outside the cell than inside, while potassium ions (K+) are more concentrated inside. The sodium-potassium pump keeps those differences in place by moving Na+ out and K+ in, and because it works against the gradients it uses energy in the form of ATP. The resting membrane is like a charged battery waiting for a switch.

Threshold and the all-or-none spike

A stimulus, such as a neurotransmitter from another cell or pressure on a touch receptor, lets some Na+ in, and the inside becomes less negative. This is depolarization. If it stays small it simply fades away. If it reaches about -55 mV, the threshold, voltage-gated sodium channels open in large numbers, Na+ rushes in and the inside climbs to about +30 mV. Then voltage-gated potassium channels open, K+ flows out and the membrane falls back. It overshoots below -70 mV for a moment, a short hyperpolarization, before settling at rest. The whole action potential takes about 2 milliseconds, and the swing from -70 to +30 is a change of 100 mV, or 0.1 volt.

Because of the threshold, an action potential is all or none. A weak stimulus that never reaches -55 mV produces no action potential at all. A strong stimulus does not make a bigger one, because every action potential peaks at the same voltage. What a stronger stimulus does is start action potentials more often. The nervous system therefore codes intensity by how frequently a neuron fires, not by how tall each spike is. During the absolute refractory period, the same membrane segment cannot initiate another action potential. This refractory period also keeps the signal moving one way, toward the axon terminals.

Rest at -70 mV. Stimulus to -55 mV, the threshold. Sodium channels open, Na+ rushes in, peak at +30 mV. Potassium channels open, K+ flows out. Overshoot below rest. Back to -70 mV.

Creeping and jumping along the axon

On an axon without myelin, the depolarization spreads a little, opens the next sodium channels, spreads a little more, and so on. This continuous conduction is slow. On a myelinated axon there are voltage-gated sodium channels only at the nodes of Ranvier. The charge spreads quickly under the myelin and the action potential is renewed at each node, so it seems to leap from node to node. This is saltatory conduction, from the Latin saltare, to leap. Wider axons also conduct faster. Thin unmyelinated fibres carry signals at roughly 0.5 to 2 metres per second; the thickest myelinated fibres reach about 120 metres per second.

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One chemical synapse, enlarged. Press Send signal, or leave Repeat on, and follow the five steps in the box. Turn on Slow motion to watch the vesicles empty.

Crossing the gap: the synapse

At the end of the axon the electrical signal has to reach another cell. A few synapses are electrical: the two cells are joined so that ions pass straight across. Most are chemical. When an action potential reaches the synaptic end bulb, voltage-gated calcium channels open and Ca2+ flows in. The calcium helps vesicles, tiny sacs full of neurotransmitter, merge with the membrane and release their contents into the synaptic cleft, the narrow gap between the cells. The neurotransmitter diffuses across and binds to receptors on the receiving cell. Receptors fit one neurotransmitter each, like a lock and a key.

Binding changes the voltage of the receiving membrane. An excitatory postsynaptic potential pushes it toward threshold; an inhibitory one pushes it away. A single input is rarely enough. Signals from many synapses, or several in quick succession from one synapse, add up at the trigger zone, and only if the total reaches threshold does the next neuron fire. Finally the neurotransmitter is cleared so the signal can end: acetylcholine is broken down by the enzyme acetylcholinesterase, and amino acids such as glutamate are pumped back into neurons or glial cells and reused. According to NINDS, acetylcholine makes muscles contract, glutamate is a major excitatory neurotransmitter and GABA is inhibitory.

BackgroundIn 1921 the pharmacologist Otto Loewi set up two beating frog hearts in separate dishes, one with its vagus nerve still attached. He stimulated the nerve and the first heart slowed, as expected. Then he moved some of the fluid bathing that heart onto the second heart, and it slowed too. Something dissolved in the fluid had carried the message. Loewi called it Vagusstoff; it was later identified as acetylcholine. He said the idea for the experiment came to him in a dream. Loewi shared the 1936 Nobel Prize with Henry Dale for discoveries about chemical transmission. The electrical side was worked out on the giant axon of the squid: in 1952 Alan Hodgkin and Andrew Huxley published their mathematical model of the action potential, and they shared the 1963 Nobel Prize with John Eccles.
Resting potentialAbout -70 mV inside, compared with outside.
ThresholdAbout -55 mV. Reach it and an action potential follows.
DepolarizationThe inside becomes less negative (Na+ enters).
RepolarizationK+ leaves and the membrane heads back toward rest.
Refractory periodTime during which a new action potential cannot start.
Saltatory conductionAction potential renewed only at nodes of Ranvier.
Synaptic vesicleSac of neurotransmitter released when Ca2+ enters.
AcetylcholinesteraseEnzyme that breaks down acetylcholine in the cleft.
  1. From the resting potential (-70 mV) to the peak (+30 mV), how many millivolts does the membrane change?
  2. How many millivolts of depolarization does it take to go from rest (-70 mV) to threshold (-55 mV)?
  3. Which ion rushes into the cell during depolarization?
    • Na+
    • K+
    • Cl-
    • Ca2+ only
  4. A stimulus twice as strong as needed for threshold produces...
    • Action potentials of the same size, more often
    • An action potential twice as tall
    • No action potential
    • A permanent depolarization
  5. What does the sodium-potassium pump do?
    • Moves Na+ out and K+ in, using ATP
    • Lets Na+ in at threshold
    • Releases neurotransmitter
    • Makes myelin
  6. Why is conduction faster on a myelinated axon?
    • The action potential is renewed only at the nodes
    • Myelin carries the ions itself
    • There are more sodium channels everywhere
    • The axon is shorter
  7. A signal travels along a 1 m axon at 100 m/s. How many milliseconds does it take?
  8. The same 1 m at 1 m/s, as on a thin unmyelinated fibre, takes how many milliseconds?
  9. What triggers vesicles to release neurotransmitter?
    • Ca2+ entering the end bulb
    • K+ leaving the cell
    • The neurotransmitter binding to receptors
    • Myelin
  10. An inhibitory postsynaptic potential...
    • Moves the membrane away from threshold
    • Always triggers an action potential
    • Opens calcium channels in the end bulb
    • Destroys the receptor
  11. Which enzyme removes acetylcholine from the synaptic cleft?
    • Acetylcholinesterase
    • ATP
    • GABA
    • Glutamate
  12. Put the events at a chemical synapse in order.
Key points
  • Resting potential about -70 mV; threshold about -55 mV; peak about +30 mV; about 2 ms in all.
  • Na+ in (depolarization), K+ out (repolarization), then a brief overshoot.
  • All or none: stronger stimuli fire more often, not bigger.
  • Myelin makes conduction saltatory: up to about 120 m/s versus about 0.5 to 2 m/s without it.
  • Chemical synapse: Ca2+ in, vesicles release, receptors bind, neurotransmitter cleared.

This is educational material about how the body is built and works. It is not medical advice and is not for diagnosing or treating anyone.

Sources for this course (11)
  • OpenStax Anatomy and Physiology 2e , 12.1 Basic Structure and Function of the Nervous System, 12.2 Nervous Tissue, 12.4 The Action Potential, 12.5 Communication Between Neurons, 13.2 The Central Nervous System, 13.4 The Peripheral Nervous System, 14.1 Sensory Perception, 14.2 Central Processing, 14.3 Motor Responses, 15.1 Divisions of the Autonomic Nervous System (openstax.org/books/anatomy-and-physiology-2e)
  • NIH NINDS "Brain Basics: Know Your Brain" and "Brain Basics: Understanding Sleep" (ninds.nih.gov/health-information/public-education/brain-basics)
  • NIH MedlinePlus "Healthy Sleep" (medlineplus.gov/healthysleep.html)
  • NIH Research Matters "Scientists build largest maps to date of cells in human brain" (nih.gov, about 86 billion nerve cells)
  • Basic Neurochemistry, Brain Energy Metabolism (ncbi.nlm.nih.gov/books/NBK28124, about 20% of the body's oxygen) and Balasubramanian 2021 "Brain power" (PMC8364152, 2% of body weight)
  • nerve conduction speeds: ScienceDirect Topics "Nerve Conduction" (myelinated up to 120 m/s, unmyelinated 0.5 to 3 m/s) and Erlanger and Gasser fibre table in "Nerve Fiber" (C fibres 0.6 to 2 m/s)
  • history: NobelPrize.org 1906 (Golgi, Cajal) and 1932 (Sherrington)
  • Tansey 1997 "Sherrington and the synapse, 1897" (PubMed 9323432)
  • PMC4291908 (Loewi 1921, Nobel 1936 with Dale)
  • PMC3424716 (Hodgkin and Huxley 1952, Nobel 1963)
  • Britannica "Broca area" (1861) and PubMed 29452328 (Leborgne, "Tan")

Checked: 2026-10-17