AnatomyAdvancedGraph simulation~15 min

Nervous System and Neuron Firing

Every thought, heartbeat signal and reflex depends on tiny electrical pulses racing along nerve cells. These pulses, called action potentials, are created by ions flowing through channels in the cell membrane. Stimulate a neuron and watch sodium and potassium channels produce a spike, using the Nobel-prize-winning Hodgkin–Huxley model.

Resting Click part of the neuron
t = 0.0 s
Stimulus type
10

Current injected into the neuron (µA/cm²). Find the weakest stimulus that still fires a spike.

1

Length of a single pulse in milliseconds.

Key

  • Na⁺ ions (flow in)
  • K⁺ ions (flow out)
  • Signal travelling down the axon
Neuron state
Resting
Membrane potential
—
Na⁺ channels open
—
K⁺ channels open
—
Action potentials
—
Conduction speed
—

Membrane potential (mV) over time (ms)

Membrane voltage of the neuron over the last 40 milliseconds, with the resting level and the threshold marked.

    Ion channel gates

    Fraction of sodium activation (m), sodium inactivation (h) and potassium activation (n) gates open over time.

      How to use this simulator

      1. Press Stimulate to inject a brief pulse of current. Time is slowed down: 5 milliseconds pass every second.
      2. Lower the stimulus strength to find the threshold — below it, the membrane barely changes; above it, a full spike fires.
      3. Press Stimulate again immediately after a spike to discover the refractory period.
      4. Choose Steady current to make the neuron fire repeatedly, and change the strength to change the firing rate.
      5. Block channels with TTX or TEA, and switch on myelin to see faster conduction. Watch both graphs below. Reset restores the resting neuron.

      Parts of a neuron

      • Dendrites receive signals from other cells.
      • The cell body (soma) contains the nucleus and combines incoming signals.
      • The axon carries action potentials away from the cell body, sometimes over a metre in humans.
      • Axon terminals release chemical messengers (neurotransmitters) to the next cell at a synapse.

      The resting potential

      A resting neuron is electrically polarized: the inside is about 65–70 mV more negative than the outside. Thisresting membrane potential exists because the sodium–potassium pump keeps Na⁺ concentrated outside and K⁺ concentrated inside, and because the resting membrane lets K⁺ leak out more easily than Na⁺ can leak in.

      The action potential

      1. Stimulus and threshold: a stimulus makes the inside less negative. If it reaches about −55 mV (threshold), the response becomes self-sustaining.
      2. Depolarization: voltage-gated Na⁺ channels open and sodium rushes in. The membrane potential shoots up to about +40 mV within a millisecond.
      3. Repolarization: Na⁺ channels inactivate, and voltage-gated K⁺ channels open. Potassium flows out and the inside becomes negative again.
      4. Hyperpolarization: K⁺ channels close slowly, so the potential briefly dips below resting (the undershoot) before recovering.

      The whole spike lasts only about 1–2 milliseconds. Remarkably few ions actually cross the membrane, so the concentration gradients barely change during a single spike.

      How the channels work

      Hodgkin and Huxley described each channel with “gates”. The sodium channel has a fast activation gate (m) that opens when the membrane depolarizes and a slower inactivation gate (h) that closes shortly afterwards. The potassium channel has a slow activation gate (n). The lower graph shows these gates: m shoots up first, then h falls and n rises — the timing difference is what creates the spike’s shape.

      Refractory periods

      Immediately after a spike, inactivated sodium channels cannot reopen, so no second spike is possible — theabsolute refractory period. A little later, a stronger-than-usual stimulus can trigger a spike — therelative refractory period. Refractoriness limits how fast a neuron can fire and makes signals travel in one direction only.

      Propagation and myelin

      An action potential in one patch of membrane depolarizes the patch next to it, which then fires too, so the spike travels down the axon like a falling line of dominoes. Many axons are wrapped in myelin, a fatty insulating layer made by glial cells. The signal then jumps between small uninsulated gaps called nodes of Ranvier — saltatory conduction — which is much faster and uses less energy. Diseases that damage myelin, such as multiple sclerosis, slow or block nerve signals.

      The Hodgkin–Huxley model

      Working with the giant axon of the squid, Alan Hodgkin and Andrew Huxley described the action potential with a set of equations in 1952, for which they shared the 1963 Nobel Prize. The simulator solves their equations directly:

      C · dV/dt = I_stim − g_Na·m³·h·(V − E_Na) − g_K·n⁴·(V − E_K) − g_L·(V − E_L)

      Here g are maximum conductances, E are the equilibrium (reversal) potentials for each ion (about +50 mV for Na⁺ and −77 mV for K⁺), and m, h and n are the gates, each changing at voltage-dependent rates.

      Key terms

      Membrane potential
      The voltage difference across the cell membrane, inside relative to outside.
      Depolarization / repolarization
      The membrane becoming less negative / returning to negative.
      Threshold
      The membrane potential at which an action potential is triggered, about −55 mV.
      Voltage-gated channel
      A protein pore that opens or closes in response to changes in membrane potential.
      Saltatory conduction
      Rapid jumping of an action potential between nodes of Ranvier on a myelinated axon.

      Real-world connections

      • Local anaesthetics such as lidocaine work by blocking sodium channels so pain signals cannot travel (educational context only).
      • Nerve toxins: tetrodotoxin from puffer fish blocks Na⁺ channels, which is why improperly prepared puffer fish can be lethal.
      • Medical tests such as nerve conduction studies and EEGs measure electrical activity from neurons.
      • Neuroscience research and brain–computer interfaces build on models like Hodgkin–Huxley.

      Common misconceptions

      • “Stronger stimuli make bigger spikes.” Spikes are all-or-none; stronger stimuli produce more frequent spikes.
      • “Nerve signals are electrons flowing like in a wire.” They are waves of ions moving across the membrane.
      • “The sodium–potassium pump makes each spike.” The pump maintains gradients over time; the spike itself is driven by channels.

      Educational model only. This simulator reproduces a classic research model of a squid axon. It is not a model of any human disease or treatment and is not medical advice. See our educational and medical disclaimer.

      Key takeaways

      • Neurons rest at about −65 to −70 mV, inside negative.
      • Reaching threshold opens Na⁺ channels (depolarization); K⁺ channels then restore the voltage (repolarization).
      • Action potentials are all-or-none and followed by refractory periods.
      • Myelin makes signals jump between nodes, greatly increasing speed.

      Knowledge check

      Nervous System and Neuron Firing: test your understanding

      Answer each question to get instant feedback and an explanation. Use the simulator to check your thinking.

      7 questions3 basic2 intermediate2 advanced

      0 of 7 answered

      1. Q1BasicWhat is the typical resting membrane potential of a neuron?
        Show answer

        Answer: C. About −70 mV

        At rest, the inside of a neuron is negative compared with the outside — about −65 to −70 mV. The simulator uses −65 mV, the value in the classic Hodgkin–Huxley model.

      2. Q2BasicWhich ions rush into the neuron during the rising phase (depolarization) of an action potential?
        Show answer

        Answer: B. Sodium (Na⁺)

        Voltage-gated sodium channels open, and Na⁺ flows in down its concentration gradient, making the inside positive. Watch the orange channels open first.

      3. Q3BasicWhat does “all-or-none” mean for an action potential?
        Show answer

        Answer: B. Once threshold is reached, a full-size spike fires; below threshold, no spike fires

        Spikes have the same size whatever the stimulus strength, as long as threshold is reached. The nervous system encodes stronger stimuli by firing spikes more often — try a steady current at different strengths.

      4. Q4IntermediateWhat causes the repolarization (falling phase) of the action potential?
        Show answer

        Answer: B. Na⁺ channels inactivating and K⁺ channels opening, so K⁺ flows out

        Sodium channels close (inactivate) on their own, while slower potassium channels open. K⁺ leaving the cell makes the inside negative again. Block K⁺ channels with TEA and see how the spike becomes much longer.

      5. Q5IntermediateWhy can’t a second action potential be triggered immediately after the first?
        Show answer

        Answer: B. During the refractory period, Na⁺ channels are inactivated and K⁺ channels are still open

        In the absolute refractory period, inactivated Na⁺ channels cannot reopen. In the relative refractory period, a stronger-than-normal stimulus is needed. This is also why signals travel in only one direction along the axon.

      6. Q6AdvancedTetrodotoxin (TTX), found in puffer fish, blocks voltage-gated Na⁺ channels. What does it do to action potentials?
        Show answer

        Answer: B. Prevents them from firing

        Without Na⁺ channels, the rising phase cannot happen, so no action potential fires however strong the stimulus. This is why TTX is extremely dangerous — it can stop the nerves that control breathing.

      7. Q7AdvancedHow does myelin speed up the signal?
        Show answer

        Answer: B. It insulates the axon so the signal jumps between gaps (nodes of Ranvier) — saltatory conduction

        Myelin prevents current leaking out, so the electrical signal spreads quickly under the insulated sections and only needs to regenerate at the nodes. Myelinated axons can conduct at up to about 100 m/s, compared with around 1 m/s for thin unmyelinated ones.

      References and further reading

      1. Betts, J. G., et al. (2022). Anatomy and Physiology 2e, Section 12.4: The Action Potential. OpenStax. openstax.org (opens in a new tab)
      2. Betts, J. G., et al. (2022). Anatomy and Physiology 2e, Section 12.2: Nervous Tissue. OpenStax. openstax.org (opens in a new tab)
      3. Hodgkin, A. L., & Huxley, A. F. (1952). A quantitative description of membrane current and its application to conduction and excitation in nerve. Journal of Physiology, 117(4), 500–544.
      4. The Nobel Prize in Physiology or Medicine 1963 — Eccles, Hodgkin and Huxley. NobelPrize.org. nobelprize.org (opens in a new tab)
      5. Purves, D., et al. (2018). Neuroscience (6th ed.), chapters on electrical signals and voltage-dependent membrane permeability. Oxford University Press.

      This page is an educational model, not medical advice. Found an error? Let us know. See our educational disclaimer.