The nervous system relies on electrical signals, known as action potentials, to communicate information rapidly across long distances. The action potential threshold is the precise electrical voltage a neuron must reach to fire this signal, acting as a “point of no return.” This threshold dictates whether communication occurs or fails. Without meeting this specific electrical requirement, any incoming signal simply fades away, making the threshold a powerful gatekeeper for all neural activity.
Setting the Stage The Resting Membrane Potential
Every neuron maintains an electrical voltage difference across its cell membrane while not actively signaling, termed the resting membrane potential. This baseline state typically sits around \(-70\) millivolts (mV), meaning the inside of the cell is negatively charged relative to the outside. This negative charge is maintained by a regulated imbalance of charged particles, specifically sodium (\(\text{Na}^{+}\)) and potassium (\(\text{K}^{+}\)) ions.
The cell membrane is much more permeable to potassium ions than to sodium ions, primarily due to leak channels that allow \(\text{K}^{+}\) to slowly diffuse out of the cell. This outward movement of positive potassium charge leaves behind negatively charged proteins inside the cell, establishing the negative voltage. The sodium-potassium pump actively maintains the concentration gradients, constantly pumping three \(\text{Na}^{+}\) ions out for every two \(\text{K}^{+}\) ions pumped in. This established negative charge is the starting line the neuron must overcome to generate an action potential.
Reaching the Critical Firing Point
A neuron receives incoming signals that cause small shifts in its membrane voltage, resulting in either depolarization (more positive) or hyperpolarization (more negative). The critical firing point, or threshold potential, is the specific voltage level required to launch a full action potential, typically between \(-55\) mV and \(-50\) mV. This threshold represents the point at which a positive feedback loop is triggered, driven by voltage-gated sodium (\(\text{Na}^{+}\)) channels.
These channels are specialized membrane proteins that remain closed at the resting potential but are highly sensitive to voltage changes. When excitatory signals depolarize the membrane from \(-70\) mV toward \(-55\) mV, a sufficient number of these \(\text{Na}^{+}\) channels quickly open. Once open, the electrochemical gradient pushes positively charged sodium ions to rush into the cell.
This rapid influx of positive charge dramatically changes the membrane voltage, causing further depolarization, which opens even more voltage-gated \(\text{Na}^{+}\) channels. This self-amplifying cascade is known as the Hodgkin cycle, which propels the membrane voltage past the threshold and up to a peak potential of about \(+40\) mV. The threshold is the precise voltage at which the inward sodium current first exceeds the outward potassium current, ensuring the signal is regenerative and self-propagating.
The All-or-None Rule of Neural Firing
The fixed action potential threshold leads directly to the all-or-none rule, which governs how neurons transmit information. This rule states that if depolarization reaches the threshold potential, a full-sized action potential will occur; if it falls short, no action potential will occur. A neuron either fires completely or does not fire at all.
The strength of the initial stimulus that pushes the neuron past the threshold does not change the amplitude or size of the resulting action potential. For example, a stimulus that barely reaches \(-55\) mV will produce an electrical spike identical in magnitude to one caused by a stronger stimulus that rapidly pushes the voltage to \(-50\) mV. The action potential is a standard size because it is generated by the uniform opening of voltage-gated channels, which always results in the same maximum influx of \(\text{Na}^{+}\) ions.
Instead of encoding information by the size of the spike, the nervous system uses the frequency of firing to communicate stimulus intensity. A weak sensory input, such as a light touch, may cause a neuron to fire action potentials at a low rate. Conversely, an intense stimulus, like a painful pinch, causes the neuron to fire a rapid burst of identical, maximal spikes. This digital signaling strategy ensures information is transmitted without losing strength over distance.
Adjusting Neural Sensitivity
The action potential threshold is not static and can be adjusted by internal and external factors, altering a neuron’s overall excitability. Changes in the concentration of ions outside the cell membrane can significantly shift the threshold. For instance, a decrease in extracellular calcium ion concentration can make the voltage-gated \(\text{Na}^{+}\) channels more sensitive, causing them to open at a more negative voltage and thus lowering the threshold. This hyperexcitability can lead to involuntary muscle spasms or seizures.
Conversely, some substances can raise the threshold, making it harder for a neuron to fire. Local anesthetics, such as lidocaine, function by physically blocking the voltage-gated \(\text{Na}^{+}\) channels, preventing the sodium influx required to cross the threshold. By raising the threshold significantly, these drugs effectively stop pain-sensing neurons from generating action potentials, blocking the transmission of pain signals to the brain. The density and subtype of voltage-gated channels present in a neuron also influence its threshold, allowing different types of neurons to have varying levels of sensitivity.