The action potential (AP) is the fundamental electrical signal allowing communication within the nervous system. This rapid change in electrical potential across a neuron’s membrane transmits information along the axon. The AP is an “all-or-nothing” event, firing completely once a specific threshold is reached. A defining characteristic is its strict directionality, traveling only forward from the cell body to the axon terminal. This movement is enforced by precise biological mechanisms that prevent the signal from doubling back.
How the Electrical Signal Moves Forward
An action potential begins with the neuron at a resting membrane potential, typically around \(-70\) millivolts (mV). When a stimulus causes the membrane potential to depolarize and reach a threshold value, usually around \(-55\) mV, a rapid sequence of events is triggered. This threshold causes the opening of voltage-gated sodium (\(\text{Na}^+\)) channels in that localized segment of the axon.
The opening of \(\text{Na}^+\) channels allows a massive influx of positively charged sodium ions into the axon. This swift movement causes the membrane potential to quickly spike, reversing the polarity to a positive value (depolarization). The \(\text{Na}^+\) influx creates a local electrical current that spreads passively to the adjacent section of the axon membrane.
This localized current raises the voltage in the next segment, bringing its voltage-gated \(\text{Na}^+\) channels to the threshold. As these channels open, depolarization is regenerated in a forward-moving wave, ensuring the signal progresses down the axon. Following the \(\text{Na}^+\) influx, voltage-gated potassium (\(\text{K}^+\)) channels open, allowing \(\text{K}^+\) ions to flow out. This efflux quickly restores the negative resting potential (repolarization).
The Absolute Barrier to Backward Travel
The refractory period, which immediately follows depolarization, strictly enforces the one-way travel of the action potential. This period is divided into two phases, starting with the absolute refractory period (ARP), which acts as the physical barrier to backward movement. During the ARP, voltage-gated \(\text{Na}^+\) channels that just opened are physically inactivated.
The \(\text{Na}^+\) channel includes an inactivation gate, often described as a tethered plug, which swings into the channel opening shortly after it opens. While this gate is in place, the channel cannot be opened again, regardless of the stimulus strength. Because the axon segment immediately behind the traveling AP has its \(\text{Na}^+\) channels blocked, the local current spreading backward cannot trigger a new depolarization.
This temporarily “shut-down” state ensures the action potential only stimulates the excitable membrane segment ahead of it. The ARP lasts for a brief duration, typically a millisecond, allowing the signal to move forward and the membrane to begin repolarizing. Once the membrane potential returns to a negative value, the inactivation gate reopens, and the channel returns to its closed, resting state.
The relative refractory period (RRP) follows the ARP, allowing an action potential to be generated only if a significantly stronger stimulus is applied. During the RRP, voltage-gated \(\text{K}^+\) channels remain open longer, leading to temporary hyperpolarization where the membrane potential becomes more negative than the standard resting potential. This greater negative charge means the cell is further from the threshold, making it less excitable. The hyperpolarized state ensures that only a strong stimulus can overcome the resistance and initiate a subsequent signal.
Structural Influences on Propagation Speed
While the refractory period determines direction, the physical structure of the axon significantly influences propagation speed. One effective strategy for increasing signal speed is myelination, where glial cells wrap the axon in a fatty insulating layer. This myelin sheath prevents charge leakage, allowing the local current to travel further down the axon before dissipating.
The myelin sheath is not continuous but is interrupted at regular intervals by exposed patches known as the Nodes of Ranvier. Voltage-gated \(\text{Na}^+\) channels are heavily concentrated only at these nodes. The action potential does not propagate continuously but “jumps” from one node to the next. This rapid skipping, called saltatory conduction, allows the signal to travel at speeds up to \(150\) meters per second, a major increase over unmyelinated axons.
Another factor influencing conduction speed is the axon’s diameter. Larger diameter axons conduct action potentials faster because they offer less internal resistance to the local current flow. The wider internal space allows positive ions to travel down the axon more easily. This reduced resistance means the current can spread further and reach the next excitable segment faster, contributing to the overall speed of signal transmission.