An action potential represents a rapid, temporary shift in the electrical charge across a cell’s membrane. This fundamental electrical signal allows for swift communication within the body, serving as the basis for nerve impulse transmission and muscle contraction. It involves a precise sequence of ion movements that momentarily reverse the cell’s electrical polarity before restoring it.
The Resting State
Before an action potential, a neuron maintains a resting membrane potential around -70 millivolts (mV). This negative charge inside the cell is due to an uneven distribution of ions across the membrane: sodium (Na+) and chloride (Cl-) are more concentrated outside, while potassium (K+) and large, negatively charged proteins are more concentrated inside.
The cell membrane is selectively permeable due to ion channels. At rest, it is most permeable to potassium (K+) through “leak” channels, allowing K+ to diffuse out. This outward movement of positive charge contributes to the internal negativity. Though some sodium (Na+) leak channels exist, the membrane’s permeability to Na+ at rest is much lower compared to K+.
Triggering the Signal: Depolarization
An action potential begins with depolarization, where a stimulus causes the neuron’s membrane potential to become less negative. This initial depolarization, often from neurotransmitters opening ion channels, must reach a “threshold potential” around -55 mV for an action potential to fire.
Once the threshold is met, voltage-gated sodium (Na+) channels rapidly open. This allows a swift influx of Na+ ions into the cell, driven by the electrochemical gradient, causing the membrane potential to quickly reverse and become positive, peaking around +30 mV. This rapid rising phase follows an “all-or-none” principle: if the threshold is reached, a full action potential will occur, regardless of stimulus strength.
Resetting the Signal: Repolarization and Undershoot
At the peak of depolarization (+30 mV), voltage-gated sodium channels rapidly inactivate, closing and preventing further Na+ influx. Simultaneously, voltage-gated potassium (K+) channels open more slowly. These channels allow K+ ions to flow out of the cell, causing the membrane potential to return to a negative value, a process called repolarization. This outward flow of potassium ions is the falling phase of the action potential.
The voltage-gated potassium channels remain open longer, leading to a brief “undershoot” or “hyperpolarization” where the membrane potential becomes even more negative than the resting potential. During this time, the membrane potential might dip to -80 mV. The state of these channels also dictates the refractory periods: an “absolute refractory period” immediately follows, during which sodium channels are inactivated and another action potential cannot be generated. This is followed by a “relative refractory period,” where a stronger-than-normal stimulus is required to trigger another action potential because some potassium channels are still open, making it harder to depolarize the membrane to threshold.
Restoring Balance
While repolarization restores the negative membrane potential, ion concentrations are temporarily altered, with more Na+ inside and K+ outside. To re-establish the original ion gradients, the sodium-potassium pump (Na+/K+-ATPase) becomes active. This active transport protein uses ATP energy to move three sodium ions out of the cell for every two potassium ions it moves back in.
This constant pumping works against the concentration gradients, maintaining low internal sodium and high potassium. By actively transporting these ions, the sodium-potassium pump restores the electrochemical balance, preparing the neuron to fire another action potential when a new stimulus arrives.