The neuron, the fundamental unit of the nervous system, communicates by generating rapid electrical signals. This communication relies on a brief, controlled shift in the electrical charge across the cell membrane, known as the membrane potential. Depolarization is the specific process where this internal charge rapidly becomes less negative, moving toward or beyond zero. This electrical shift is the primary mechanism that allows a neuron to transmit information along its length and throughout the nervous system.
Establishing the Resting Membrane Potential
For a neuron to fire an electrical signal, it must maintain a steady, negative electrical charge when at rest. This baseline charge, around -70 millivolts (mV), is called the resting membrane potential. This potential is established by an unequal distribution of positively and negatively charged ions, primarily sodium (Na+) and potassium (K+), across the cell’s membrane.
The concentration gradients for these ions are actively maintained by the sodium-potassium pump, a protein complex embedded in the cell membrane. This pump continuously uses energy to transport three sodium ions out of the cell for every two potassium ions it brings in. This action creates a high concentration of sodium outside the neuron and potassium inside, setting up the necessary imbalance for electrical activity.
The resting negativity is largely due to non-gated, or “leak,” potassium channels that are always open. Since potassium is highly concentrated inside the cell, these channels allow positive potassium ions to slowly leak out. This constant outward flow, combined with large, negatively charged proteins trapped inside, causes the internal environment to remain negative relative to the outside.
The Mechanism of Depolarization
Depolarization is the shift of the membrane potential from its negative resting state toward a less negative or even a positive value. This process is triggered when the neuron receives a stimulus, causing a small, initial change in the membrane voltage. If this initial depolarization is large enough to reach the threshold potential, an action potential is unleashed.
The threshold potential is usually between -55 mV and -50 mV, marking the point of no return for the neuron. Reaching this voltage causes voltage-gated sodium channels to rapidly open, initiating depolarization. Since sodium ions are highly concentrated outside the cell and attracted by the negative charge inside, they rush into the neuron down a steep electrochemical gradient.
This massive influx of positively charged sodium ions drives the rapid spike in voltage, momentarily reversing the electrical charge across the membrane. The internal charge can quickly rise from the threshold of -55 mV up to a positive value, often peaking around +30 mV. This rapid change operates on an “all-or-nothing” principle: if the threshold is not met, no action potential fires, but if it is met, the full signal always fires with the same intensity.
Completing the Cycle: Repolarization and Hyperpolarization
The depolarizing spike is brief and must be followed immediately by a process to restore the membrane’s resting negative charge. This restorative process is called repolarization, which begins instantly after the membrane potential peaks at its most positive value. Repolarization is initiated by two simultaneous actions involving voltage-sensitive ion channels.
First, the voltage-gated sodium channels that caused the depolarization rapidly inactivate; they close and cannot be immediately reopened. This action stops the influx of positive sodium ions, preventing the charge from remaining positive. Second, a different set of voltage-gated potassium channels, which open more slowly than the sodium channels, fully open.
With the potassium channels open and the sodium channels closed, positively charged potassium ions rush out of the cell, driven by their high internal concentration. This outward flow quickly returns the internal membrane potential toward its negative resting state. However, the potassium channels are delayed in closing, causing a brief period called hyperpolarization. During hyperpolarization, the membrane potential dips even more negative than the resting potential, creating an “undershoot.” This period is part of the refractory phase, which temporarily makes it more difficult for the neuron to fire a second action potential, ensuring signals move in one direction.
How Depolarization Enables Neural Communication
The localized depolarization event, or action potential, serves as the signal that travels the length of the neuron’s axon. The influx of positive sodium ions at one point spreads to adjacent areas, causing the voltage-gated sodium channels there to reach their threshold and open. This sequential opening and closing of ion channels allows the electrical signal to propagate rapidly down the axon without losing strength.
When this traveling wave of depolarization reaches the axon terminal, it triggers the next stage of communication. The change in voltage at the terminal opens voltage-gated calcium channels. The resulting influx of calcium ions causes small membrane-bound sacs, known as synaptic vesicles, to fuse with the cell membrane.
The fusion of these vesicles releases chemical messengers called neurotransmitters into the synaptic cleft, the small gap between neurons. These chemicals diffuse across the cleft to bind with receptors on the next neuron, potentially causing a new depolarization and continuing the signal’s journey. Thus, the initial depolarization event is translated from an electrical signal within one neuron into a chemical signal that excites the next cell in the circuit.