Action Potential Simulations

An Exploration of Neuron Membrane Physiology

Action Potential Phases

Introduction

An action potential begins when a stimulus depolarizes the neuron’s cell membrane from the resting potential of -70 mV to the threshold of approximately −55 mV, triggering a rapid and predictable sequence of electrical events that can be divided into three distinct phases: depolarization, repolarization, and hyperpolarization.

Two types of voltage-gated channel proteins in the axon membrane regulate these changes in membrane potential: Na⁺ voltage-gated channels and K⁺ voltage-gated channels. As their names suggest, these channels are sensitive to changes in membrane potential and open once the threshold is reached.

The Na⁺ voltage-gated channel has two gates: an activation gate and an inactivation gate. The K⁺ voltage-gated channel has only one gate: an activation gate.

Resting: Channel States

At rest, most voltage-gated Na⁺ and K⁺ activation gates are closed, but the channels are available to respond to a threshold-level stimulus. In voltage-gated Na⁺ channels, the inactivation gate is open/non-blocking. This means the Na⁺ channel is closed at rest, but ready to open when a threshold stimulus is reached.

Na+ voltage-gated channel with the activation gage closed and the inactivation gate open/non-blocking
K+ voltage-gated channel with theactivation gage closed

Depolarization Phase: Channel States

A threshold-level stimulus affects both types of voltage-gated channels, but Na⁺ channels respond first. Their activation gates open rapidly, allowing Na⁺ ions to enter the cell down their electrochemical gradient. As positive charges enter the cell, the membrane depolarizes and overshoots 0 mV to approximately +30 to +40 mV.

Na+ voltage-gated channel with the activation gage open and the inactivation gate open/non-blocking
K+ voltage-gated channel with theactivation gage closed

Repolarization Phase: Channel States

Depolarization ends when the Na⁺ inactivation gates move into a blocking position. This time-dependent response to the earlier threshold stimulus prevents continued Na⁺ entry through most voltage-gated Na⁺ channels, even though the membrane remains depolarized. As more Na⁺ channels become inactivated, Na⁺ influx decreases, and further depolarization stops.

By this stage, the slower voltage-gated K⁺ channels have begun to open, allowing K⁺ ions to efflux (move outward) down their electrochemical gradient. Repolarization begins when outward K⁺ movement exceeds inward Na⁺ movement, causing the membrane potential to move back toward more negative values.

Na+ voltage-gated channel with the activation gage open and the inactivation gate closed/blocking
K+ voltage-gated channel with the activation gage open

Hyperpolarization Phase

Because voltage-gated K⁺ channels close slowly, K⁺ continues to leave the cell after repolarization. This continued K⁺ efflux briefly makes the inside of the membrane more negative than its resting level, producing hyperpolarization, or an undershoot, to about −80 to 90 mV. During repolarization and hyperpolarization, the return toward a more negative membrane potential causes Na⁺ activation gates to close and Na⁺ inactivation gates to move back into their open, non-blocking position.

Na+ voltage-gated channel with the activation gage closed and the inactivation gate open/non-blocking
K+ voltage-gated channel with the activation gage open

Return To Resting State

As voltage-gated K⁺ channels close, the extra outward movement of K⁺ decreases, so the membrane is no longer driven further into hyperpolarization. The same mechanisms that establish and maintain the resting membrane potential, especially K⁺ leak channels and the Na⁺/K⁺ pump, return the membrane to its resting state and maintain the Na⁺ and K⁺ gradients over time.

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Analysis / Quiz
An action potential was triggered when a stimulus depolarized the membrane to approximately −55 mV.
Na⁺ moves into the axon down its electrochemical gradient. Na⁺ is more concentrated outside the axon, and the inside of the axon is relatively negative, so both forces drive Na⁺ inward.
Most voltage-gated Na⁺ channels respond to threshold by opening their activation gates, which allows Na⁺ ions to enter the axon.
Depolarization lasted about 1 millisecond and reached a peak membrane potential of approximately +40 mV.
Most voltage-gated K⁺ channels remain closed during early depolarization because they open more slowly than Na⁺ channels. This matters because Na⁺ influx can rapidly depolarize the membrane before K⁺ efflux begins to oppose it.
Repolarization lasted about 1 ms. During this time, the membrane potential fell from about +40 mV to near resting potential.
At the peak of the action potential, the inactivation gates of most voltage-gated Na⁺ channels close and block the channel pore. This stops most Na⁺ entry. At the same time, voltage-gated K⁺ channels are opening, so K⁺ begins leaving the cell and the membrane starts to repolarize.
The activation gate is open, but the channel is blocked by the inactivation gate. The channel cannot conduct Na⁺ again until the membrane repolarizes, allowing the gates to reset to their original resting state.
Voltage-gated K⁺ channels are open or continuing to open during repolarization, allowing K⁺ ions to flow out of the axon down their electrochemical gradient. Because K⁺ carries positive charge out of the cell, the inside of the axon becomes less positive and the membrane potential falls back toward −70 mV.
Voltage-gated K⁺ channels are slow to close. They continue to allow K⁺ to leave the axon even after the membrane potential returns near −70 mV. This continued K⁺ efflux causes the membrane potential to overshoot below resting level, briefly reaching about −80 to −90 mV.
During hyperpolarization, many voltage-gated Na⁺ channels are recovering from inactivation. Their inactivation gates reset to the non-blocking position, and their activation gates close. As this reset occurs, the channels return to their resting state and become available for a future action potential.
The rapid opening of voltage-gated Na⁺ channels causes depolarization. Na⁺ channel inactivation and the opening of voltage-gated K⁺ channels cause repolarization. Because K⁺ channels close slowly, K⁺ continues to leave the axon and produces hyperpolarization.

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Reference and Attributions

BioPhysiology – “The Action Potential“.

Cellular Neurophysiology – “Synaptic Transmission in the Central Nervous System“.

Integrated Human Anatomy and Physiology – “The Action Potential“.

Khan Academy – “Neuron action potentials“.

Michigan State U. – “Action Potentials“.

Monash University – “Action Potential Experiments.“

Georgia Tech Biological Sciences – “Neurons.”

OpenStax, Anatomy and Physiology – “The Action Potential“. Access for free at – https://openstax.org/books/anatomy-and-physiology/pages/1-introduction

PhysioWeb – “Neuronal Action Potential“.

ResearchGate – “Mathematical modeling of neurovascular coupling“.

ResearchGate – “Onset Dynamics of Action Potentials in Rat Neocortical Neurons and Identified Snail Neurons: Quantification of the Difference“.

ScienceDirect – “Action Potential“.

ScienceDirect – “Spatial Summation“.

ScienceDirect – “Threshold Potential“.

UEN Integrated Human Anatomy and Physiology – “The Action Potential“

University of Sussex – ” Neuronal Transmission“.

Wikipedia – “Hodgkin–Huxley model“.

Wikipedia – “The Action Potential“.

Wikipedia – “Summation (neurophysiology)“.