Ion Gradients Drive the Neuron Action Potential
Inside a glowing neuron axon magnified to room scale, Medi crouches beside a giant membrane panel studded with glowing channel proteins, pressing a voltage meter probe against the lipid bilayer while sparks of sodium ions rush through a freshly opened gate.
- Explain why a neuron at rest maintains a negative membrane voltage near -70 mV.
- Describe the sequential opening of voltage-gated sodium and potassium channels during an action potential.
- Identify the all-or-none principle and explain why threshold voltage is the critical trigger.
- Compare depolarization, repolarization, and hyperpolarization in terms of ion movement and membrane voltage.
- Predict how blocking sodium or potassium channels would alter the action potential waveform.
Key terms
- Resting membrane potential
- The steady voltage (~-70 mV) across a neuron membrane when it is not firing, set by ion gradients and the Na⁺/K⁺ pump.
- Threshold
- The critical membrane voltage (~-55 mV) at which voltage-gated sodium channels open en masse and an action potential becomes unavoidable.
- Depolarization
- The phase in which inward Na⁺ flow drives the membrane voltage rapidly toward positive values, peaking near +30 mV.
- Repolarization
- The phase in which outward K⁺ flow returns the membrane voltage back toward its negative resting value.
- Refractory period
- A brief interval after the spike when a neuron cannot fire again (absolute) or requires a stronger stimulus (relative).
The Resting State as Stored Energy
The -70 mV resting potential is not passive equilibrium but a poised, energy-requiring state. The Na⁺/K⁺-ATPase exports 3 Na⁺ for every 2 K⁺ imported, building steep concentration gradients while removing net positive charge from the interior. K⁺ leak channels let potassium drift out down its gradient, and trapped intracellular anions add negativity. Together these establish the electrochemical 'battery' whose stored potential energy is released, all at once, when the cell finally fires.
Channel Kinetics Set the Waveform
The action potential's shape reflects the differing kinetics of two channel types. Voltage-gated Na⁺ channels open fast and then self-inactivate within about a millisecond via an inactivation gate, ending depolarization regardless of voltage. Voltage-gated K⁺ channels open more slowly and stay open longer, driving repolarization and the brief hyperpolarizing undershoot. Because Na⁺ channels stay inactivated until the membrane re-polarizes, the absolute refractory period guarantees one-way propagation and caps the maximum firing frequency.
Worked examples
Trace the membrane voltage and channel states as a neuron fires once from rest.
- Start at -70 mV: Na⁺/K⁺ pump and K⁺ leak hold the resting potential; both voltage-gated channels are closed.
- A stimulus depolarizes the membrane to -55 mV (threshold), triggering voltage-gated Na⁺ channels to open together.
- Na⁺ floods inward down its electrochemical gradient, sending voltage toward +30 mV (depolarization).
- Na⁺ channels inactivate and slow K⁺ channels open; K⁺ exits and voltage falls (repolarization).
- K⁺ channels close late, so voltage briefly undershoots to ~-80 mV (hyperpolarization) before the pump restores -70 mV.
Answer: One all-or-none spike: rest (-70) → threshold (-55) → peak (+30) → repolarize → hyperpolarize (-80) → rest (-70).
Predict the effect of a sodium-channel-blocking local anesthetic on the spike.
- Identify the role of voltage-gated Na⁺ channels: they carry the inward current that produces depolarization.
- If the blocker prevents these channels from opening, threshold may be reached but no regenerative Na⁺ influx follows.
- Without depolarization there is no propagating action potential, so the signal cannot be transmitted.
Answer: No action potential fires; signal conduction is blocked (the basis of local anesthesia such as lidocaine).
Activity
Drag each event onto the correct position on the action potential timeline, from resting state through hyperpolarization.
Practice
If a toxin permanently locks voltage-gated Na⁺ channels in the inactivated state, predict what happens to the neuron's ability to fire and explain why.
Explain why the action potential is described as 'all-or-none' and how this differs from a graded potential at a dendrite.
Common mistakes to avoid
- Bigger stimuli produce bigger action potentials.Once threshold is reached the spike is fixed in size; stronger stimuli instead raise firing frequency, not amplitude.
- The Na⁺/K⁺ pump directly causes the action potential spike.The pump only maintains the gradients beforehand; the spike itself is driven by voltage-gated Na⁺ and K⁺ channels opening.
Check your understanding
A neuron receives a stimulus that raises its membrane voltage from -70 mV to -60 mV but threshold is -55 mV. What will happen?
Which ion movement is primarily responsible for the rapid depolarization phase of the action potential?
A drug blocks voltage-gated potassium channels without affecting sodium channels. How would this most likely alter the action potential?
Recap
A neuron rests near -70 mV because of ion gradients maintained by the Na⁺/K⁺ pump. At threshold, voltage-gated Na⁺ channels open for all-or-none depolarization, then inactivate as slower K⁺ channels repolarize and briefly hyperpolarize the membrane before the next signal.
Reflect
Where in this loop does the cell spend metabolic energy, and where does it instead exploit gradients it already built?