Electrical excitability is a property of specific cells, primarily neurons and muscle cells, that allows them to respond to stimulation with a rapid electrical signal. It can be thought of like a biological light switch; a sufficient stimulus flips the switch, causing the cell to transition from a resting to an active state. This capability is a specialized function of cells involved in communication and movement.
The Cellular Basis of Excitability
A cell’s electrical excitability is built upon its electrochemical environment. Every excitable cell is enclosed by a plasma membrane separating its interior fluid from the outside. In its resting state, the inside of the cell holds a stable, negative electrical charge relative to the outside. This stored electrical difference is the resting membrane potential, which sits around -65 to -70 millivolts in neurons.
This potential is like a charged battery, ready to discharge. The charge is established by different concentrations of ions on either side of the membrane, with a high concentration of potassium ions inside the cell and sodium ions outside. These gradients are actively managed by the sodium-potassium pump, which moves three sodium ions out of the cell for every two potassium ions it brings in.
Embedded within the cell membrane are specialized pores known as ion channels. Many of these are “voltage-gated,” meaning they open when the cell’s voltage changes from its resting potential. These channels are selective, with some allowing only sodium ions to pass through and others specific to potassium ions. In the resting state, the membrane is mostly impermeable to sodium but slightly permeable to potassium through leak channels, which helps establish the negative interior charge.
The Action Potential
The action potential is a brief, all-or-nothing electrical impulse that allows a cell to “fire.” This process is initiated when a stimulus, like a chemical signal from another neuron, causes a slight change in the membrane potential. For an action potential to occur, this stimulus must be strong enough to push the membrane potential from its resting value to a “threshold” level, around -55 mV.
Once the threshold is reached, the event proceeds automatically in a phase called depolarization. Voltage-gated sodium channels open, and because of the high concentration of sodium ions outside and the negative charge inside, sodium ions rush into the cell. This causes a rapid reversal of the membrane potential, with the inside becoming positive to about +30 mV. This phase is very fast, lasting about one millisecond in neurons.
Following the peak, the cell resets itself in a phase called repolarization. The voltage-gated sodium channels that drove depolarization inactivate, stopping the influx of sodium. At the same time, voltage-gated potassium channels open, and since potassium is highly concentrated inside the cell, these positive ions rush out. This outflow restores the negative potential, though it often briefly becomes more negative than the resting state (hyperpolarization) before the sodium-potassium pump restores the original ion balance.
Following an action potential is a brief interval known as the refractory period. During the first part, the absolute refractory period, the sodium channels are inactivated and cannot be opened again. This makes it impossible for another action potential to be generated. This ensures the electrical signal is a discrete event and forces it to travel in one direction.
Propagation of the Signal
An action potential generated at one location must travel to communicate a signal. In unmyelinated axons, this propagation occurs like a continuous wave. The depolarization in one segment creates a local electrical current that spreads to the adjacent segment. This raises its potential to the threshold, triggering a new, identical action potential, a process that repeats along the axon like falling dominoes.
To increase signal speed, many vertebrate axons are wrapped in an insulating layer called a myelin sheath. This sheath is not continuous but has small, exposed gaps at regular intervals called the nodes of Ranvier. These nodes are densely packed with the voltage-gated ion channels necessary to generate an action potential. Myelin insulates the axon, preventing ion leakage and allowing the current to travel rapidly from one node to the next.
This arrangement allows the action potential to “jump” from node to node, a process known as saltatory conduction. Instead of being regenerated at every point, the signal is only renewed at these gaps. This method of propagation is faster and more energy-efficient than continuous conduction. Signals in myelinated axons can travel at speeds up to 150 meters per second, compared to 0.5 to 10 m/s in unmyelinated ones.
Functional Roles in the Body
In the nervous system, electrical excitability is the basis of all communication. Action potentials traveling along neurons allow for the rapid transmission of information from sensory organs to the brain. They also enable the processing of thoughts and memories, and the sending of commands from the brain to the rest of the body.
In the muscular system, electrical signals trigger contraction. Skeletal muscles, responsible for voluntary movements, depend on signals from the nervous system to function. An action potential traveling down a motor neuron causes the release of chemical messengers that trigger a corresponding action potential in the muscle fiber, initiating contraction. Smooth and cardiac muscle also rely on excitability, though they can respond to other stimuli like hormones as well.
The rhythmic beating of the heart is controlled by specialized cardiac muscle cells known as pacemaker cells. These cells spontaneously generate action potentials that propagate throughout the heart muscle in a sequence. This triggers the coordinated contractions of the atria and ventricles that pump blood. This autorhythmicity ensures the heart continues to function, while signals from the nervous system can modulate the rate to meet the body’s needs.
When Excitability Goes Wrong
Disruptions in electrical excitability can lead to significant disorders. Many of these conditions, sometimes called channelopathies, arise from mutations in the genes that build ion channels. For example, some forms of epilepsy are characterized by excessive, synchronized electrical firing in brain neurons, leading to seizures. This can be caused by genetic variants affecting sodium channels.
In the heart, problems with electrical signaling can cause cardiac arrhythmias, where the heart beats too fast, too slow, or irregularly. Mutations in the SCN5A gene, which encodes a sodium channel in the heart, are linked to inherited arrhythmia syndromes that can increase the risk of sudden cardiac death. These mutations alter the function of the channels, disrupting the timing of the heart’s electrical impulses.
External substances can also interfere with electrical excitability. Tetrodotoxin, a neurotoxin found in pufferfish, blocks certain voltage-gated sodium channels. By preventing sodium from entering nerve and muscle cells, the toxin inhibits their ability to fire action potentials. This blockage leads to muscle paralysis and can be fatal by causing respiratory failure.