Nerve cells, or neurons, are the communication specialists of the body, transmitting information using rapid electrical signals known as action potentials. An action potential is a brief electrical pulse that travels down a neuron, serving as the fundamental unit of information for nerve and muscle cells. This signal allows for complex processes from thought to movement. Understanding how this pulse is formed and how the neuron resets after it passes is key to understanding nervous system function.
The Action Potential Cascade
In its resting state, a neuron maintains a stable negative charge across its membrane, known as the resting membrane potential. This charge, typically around -70 millivolts, is established by maintaining different concentrations of ions, particularly sodium (Na+) and potassium (K+). The outside of the neuron has a high concentration of sodium ions, while the inside has a high concentration of potassium ions, creating a state of readiness.
The process begins when a neuron receives a stimulus, often a chemical message from another neuron, causing a disturbance in the membrane that makes it less negative. If this change is strong enough to reach a “threshold potential” of around -55 mV, it triggers an action potential. Reaching this threshold initiates an all-or-nothing event; the action potential will fire completely or not at all.
Once the threshold is crossed, voltage-gated sodium channels open. Because of the high concentration of sodium ions outside the cell, Na+ ions flood into the neuron. This influx of positive charge rapidly reverses the membrane’s polarity to a positive value of about +30 or +40 mV. This rapid upswing is the rising phase, or depolarization, of the action potential.
The Mechanism of Repolarization
At the peak of the action potential, the neuron begins the process of returning to its negative resting state. This is initiated by two coordinated events. First, the voltage-gated sodium channels that caused depolarization undergo inactivation, where a part of the channel protein physically blocks the pore. This prevents any more sodium from entering the cell and is a temporary state, distinct from the channels simply being closed.
Simultaneously, a different set of channels, the voltage-gated potassium channels, fully open. These channels also respond to the initial depolarization but do so more slowly than their sodium counterparts. By the time the action potential reaches its peak, these potassium channels are wide open, creating a pathway for potassium ions (K+) to move across the membrane.
With the inside of the cell now strongly positive and the potassium channels open, K+ ions are driven out of the neuron. This movement is compelled by both the positive electrical charge inside the cell and the high concentration of K+ inside the cell. This outward flow of positive charge is known as efflux.
This rapid exit of potassium ions is the driving force behind repolarization, the “falling phase” of the action potential. As positive charge leaves the cell, the membrane potential plummets from its positive peak back toward the negative resting potential. The process is self-regulating, as the voltage changes caused by one set of channels trigger the actions of the next.
Resetting the System
The process of resetting the neuron for the next signal begins immediately after repolarization and involves a brief overcorrection. The voltage-gated potassium channels that drive repolarization are slow to close, even after the membrane potential has returned to its resting level. This allows extra potassium ions to leak out, causing the membrane potential to dip more negative than its usual resting state, a phase known as hyperpolarization.
This period of hyperpolarization is linked to the neuron’s refractory period, a short interval during which it is more difficult or impossible to fire another action potential. The first part is the absolute refractory period, where the voltage-gated sodium channels are in their inactivated state and cannot be reopened. This ensures that the action potential signal propagates in only one direction down the axon.
Following this is the relative refractory period, which coincides with hyperpolarization. During this time, the sodium channels have returned to their resting state, but a new action potential is harder to trigger because the membrane is more negative than usual. A stronger-than-normal stimulus is required to reach the threshold, which helps regulate the frequency of firing.
While ion channels manage the rapid changes during an action potential, the long-term maintenance of ion balance is handled by the sodium-potassium pump. This protein uses energy (ATP) to actively transport sodium ions out of the cell and potassium ions back in. This pump ensures that the concentration differences needed for neuronal signaling are preserved after countless action potentials.
Significance in Bodily Function
The precise timing of repolarization is important to the function of the nervous system. The rapid reset allows neurons to fire signals in quick succession, with some able to generate hundreds of action potentials per second. This high-frequency firing is necessary for encoding the intensity of a stimulus and for carrying out complex operations like sensory processing and motor commands. Without efficient repolarization, communication between neurons would be slow.
In the cardiovascular system, repolarization is important for maintaining a regular heartbeat. The action potentials in cardiac muscle cells are longer than in neurons, and the duration of the repolarization phase determines the heart’s contraction and relaxation cycle. A properly timed repolarization ensures that the heart chambers have sufficient time to fill with blood before the next beat.
Disruptions to the repolarization process can have health consequences. Genetic conditions known as channelopathies, which involve mutations in the genes that build ion channels, can impair the flow of ions. For example, Long QT syndrome is a disorder where faulty potassium channels slow down repolarization in the heart. This delay increases the risk of irregular heart rhythms (arrhythmias), which can lead to fainting or cardiac arrest.