The neuron is the fundamental cell of the nervous system, responsible for transmitting information throughout the body. This communication relies on a rapid, momentary shift in electrical voltage across the cell membrane, known as the action potential. This electrical signal allows neurons to communicate across long distances, enabling swift and coordinated responses. The process operates under an “all-or-nothing” principle, meaning that once triggered, the signal proceeds fully and uniformly.
Establishing the Baseline Electrical State
A neuron not actively transmitting a signal maintains a stable internal electrical charge, referred to as the Resting Membrane Potential (RMP). This resting state typically measures approximately \(-70\) millivolts (\(\text{mV}\)), meaning the inside of the cell is negative relative to the outside. This charge separation is maintained by an uneven distribution of charged particles, or ions, across the cell membrane.
The concentration gradients for sodium (\(\text{Na}^+\)) and potassium (\(\text{K}^+\)) ions primarily determine the RMP. Sodium ions are highly concentrated outside the neuron, while potassium ions are highly concentrated inside. The cell membrane possesses more open “leak” channels for potassium, allowing positive potassium ions to slowly diffuse out and pull the internal charge toward a negative value.
The Sodium-Potassium (\(\text{Na}^+/\text{K}^+\)) pump actively maintains these necessary gradients against diffusion. This protein complex uses energy to continuously transport three \(\text{Na}^+\) ions out of the cell for every two \(\text{K}^+\) ions it brings in. This unequal exchange contributes to the negative RMP and ensures the high concentration gradients are ready for the neuron to fire.
The Step-by-Step Firing Sequence
The action potential begins when a stimulus causes the neuron’s membrane potential to shift from \(-70\text{ mV}\) toward a less negative value. If this depolarization reaches the threshold voltage, typically around \(-55\text{ mV}\), the neuron rapidly initiates the full firing sequence. Reaching the threshold causes a swift change in the membrane’s permeability to ions, transforming the cell’s electrical state.
The rising phase, or depolarization, is triggered by the opening of voltage-gated sodium channels. These channels are sensitive to voltage changes and allow positively charged \(\text{Na}^+\) ions to rush into the cell, driven by electrical and concentration gradients. This rapid influx of positive charge causes the membrane potential to swing dramatically, often peaking at about \(+30\text{ mV}\), where the inside of the cell briefly becomes positive.
This peak voltage causes the sodium channels to quickly inactivate and simultaneously triggers the slower opening of voltage-gated potassium channels. The repolarization phase follows, as the positively charged \(\text{K}^+\) ions rush out. This efflux of positive charge rapidly brings the membrane potential back toward its negative resting value.
As the potassium channels are slow to close, the membrane potential briefly overshoots the normal \(-70\text{ mV}\) RMP, creating a momentary hyperpolarization. This brief dip ensures the refractory period, which limits the neuron’s ability to fire again immediately. During the absolute refractory period, the inactivated sodium channels cannot be reopened, forcing the signal to travel in only one direction down the axon.
How the Signal is Transmitted Down the Axon
Once generated, the action potential must be propagated quickly down the axon to the next cell. This transmission occurs because the influx of sodium ions at one point creates an electrical current that rapidly depolarizes the adjacent segment of the axon membrane. This process repeats sequentially down the entire length of the axon, regenerating the signal as it moves.
In axons lacking a fatty insulation layer (unmyelinated axons), the signal propagates through continuous conduction. The action potential is regenerated at every point along the membrane in a smooth, wave-like fashion. This method is effective but relatively slow, as the full sequence of ion channel openings must occur step-by-step across the entire surface.
Many axons are wrapped in a Myelin sheath, a fatty tissue layer formed by glial cells that acts as an electrical insulator. This insulation prevents current leakage and forces the action potential to employ a much faster transmission method called saltatory conduction. The myelin sheath is interrupted at regular, uninsulated intervals called the Nodes of Ranvier.
Saltatory conduction, derived from the Latin word for “leaping,” describes the action potential jumping from one Node of Ranvier to the next. Voltage-gated sodium channels are highly concentrated only in these nodes. The electrical current flows passively and quickly under the myelinated segments, regenerating the full action potential only when it reaches the next node, significantly increasing transmission speed.
Action Potentials in Neurological Function and Dysfunction
The action potential mechanism is a target for many medical interventions and is implicated in certain neurological disorders. Local anesthetics, such as lidocaine, exert their effect by physically blocking the voltage-gated \(\text{Na}^+\) channels in sensory nerves. By preventing \(\text{Na}^+\) ions from rushing in, these drugs stop the nerve from reaching the threshold and block the transmission of pain signals to the brain.
Disorders that damage the Myelin sheath impair the speed and efficiency of action potential conduction. Multiple Sclerosis (MS), for instance, involves the immune system attacking and degrading myelin in the central nervous system. This demyelination slows or completely halts saltatory conduction, leading to symptoms due to delayed or failed signal transmission in affected neural pathways.
Certain neurotoxins target the ion channels responsible for the action potential, altering the body’s communication systems. For example, tetrodotoxin, found in pufferfish, works by binding to and blocking the voltage-gated sodium channels. This blockade prevents depolarization, leading to paralysis and loss of sensation by silencing the electrical signals required for muscle and nerve function.