What Is an Action Potential
An action potential is a rapid, transient reversal of the neuronal membrane potential that enables long-distance electrical signaling in neurons. At its core, this event represents the coordinated opening and closing of voltage-gated ion channels, allowing selective flow of ions across the membrane. The result is a stereotyped all-or-none depolarization followed by repolarization and a refractory period. Before an action potential can occur, the membrane must reach a specific level of depolarization known as threshold, which defines the minimum change in voltage required to initiate firing.
Defining the Threshold Stimulus
The threshold stimulus is the minimal depolarting current or input that brings the membrane potential to threshold, the critical voltage at which voltage-gated sodium channels begin to activate rapidly in a regenerative feedback loop. Below this level, only local, decremental changes occur; at or above this level, an action potential is reliably generated. The threshold is not a fixed number across all cells or conditions, but it is typically around −55 to −50 mV relative to the resting potential in many mammalian neurons. Reaching threshold normally requires sufficient net inward current carried mainly by sodium ions through ligand-gated, mechanically-gated, or voltage-gated pathways that summate in both space and time.
Spatial and Temporal Summation
Because a single subthreshold input rarely reaches threshold, neurons integrate multiple excitatory and inhibitory signals. Spatial summation combines simultaneous inputs from different synapses, while temporal summation adds inputs arriving in quick succession at the same synapse. The net effect determines whether the membrane approaches or exceeds threshold. If the summed depolarization is strong and persistent enough to reach threshold, regenerative sodium influx fires an action potential; if not, the neuron remains at rest or exhibits only local electrotonic changes. This integration is fundamental to information processing and coincidence detection in neural circuits.
How Ion Channels Create Threshold and Propagation
Voltage-gated sodium channels are the primary drivers of the upstroke of the action potential once threshold is reached. These channels open quickly in response to membrane depolarization, allowing a rapid influx of Na+ that further depolarizes the membrane in a positive feedback cycle. Subsequently, delayed rectifier potassium channels open more slowly to repolarize and hyperpolarize the membrane, restoring the negative resting state. The absolute and relative refractory periods that follow limit firing frequency and ensure directionality of signal propagation along the axon. Myelin sheaths and larger axon diameter further facilitate rapid, efficient transmission by increasing membrane resistance and reducing cable attenuation.
Stimulus Features That Determine Threshold Crossing
Not all inputs can trigger an action potential. Effective stimuli must be adequate in modality (type of energy detected by sensory receptors), intensity, and duration. For a stimulus to reach threshold, it must depolarize the membrane sufficiently to overcome the threshold voltage. Subthreshold stimuli produce graded potentials that decay with distance and time, while suprathreshold stimuli reliably initiate regenerative firing once threshold is crossed. Different neurons have different thresholds based on ion channel expression, neuromodulators, and cellular properties, allowing computation and filtering of sensory information before transmission to downstream circuits.
Modulation of Threshold and Excitability
Threshold and neuronal excitability are dynamically regulated by neuromodulators, synaptic inputs, and intrinsic membrane properties. For example, inhibitory neurotransmitters and hyperpolarizing conductances raise the effective threshold by making depolarization harder to achieve, while excitatory inputs and certain neuromodulators lower threshold by increasing background excitation or reducing accommodation. Additionally, slow changes in resting potential via ion pumps and cotransporters, along with calcium-dependent feedback, can adjust excitability over seconds to minutes. These mechanisms allow the nervous system to gate when neurons respond, providing context-dependent signal selection and preventing runaway excitation.
Measuring and Comparing Stimulus Strength
Because stimulus intensity is often encoded in the pattern of action potentials rather than in single-firing amplitude, the rate or pattern of spikes—collectively the population code—carries information about how strong a stimulus is. Below threshold, firing probability remains low; near threshold, small changes in input can produce marked changes in firing rate; well above threshold, firing saturates. Researchers commonly quantify stimulus strength using measures such as rheobase (minimum sustained current to elicit firing) and chronaxie (duration required at twice rheobase to reach threshold). These metrics offer a stable, physiologically grounded way to compare excitability across neurons and conditions.
| Attribute | Verified Detail | Source Type |
|---|---|---|
| Threshold potential (typical) | Approximately −55 to −50 mV relative to resting potential in many mammalian neurons | Electrophysiology data, textbooks |
| Primary depolarizing ion at threshold | Sodium influx through voltage-gated Na+ channels | Ion channel physiology |
| Refractory period role | Limits firing frequency and ensures one-way propagation | Experimental recordings |
| Stimulus features needed to reach threshold | Adequate modality, intensity, and duration to produce summated depolarization | Sensory physiology literature |
| Rate code for intensity | Above threshold, stronger inputs increase firing rate, not spike amplitude | Systems neuroscience |
From Subthreshold to Suprathreshold: Practical Examples
Consider a sensory neuron responding to touch: gentle pressure may produce small receptor potentials that fail to reach threshold, while stronger pressure summates spatially and temporally to trigger an action potential. In central neurons, converging excitatory postsynaptic potentials from multiple upstream cells can push a target neuron past threshold, whereas inhibitory inputs can prevent firing even when excitation is present. Clinically, altered threshold or excitability underlies phenomena such as neuropathic pain, epilepsy, and certain channelopathies, highlighting the importance of precise threshold control for reliable signaling.
Why This Matters for Understanding Neural Coding
Recognizing that only supra-threshold stimuli consistently generate action potentials clarifies how neurons balance sensitivity and noise. It also explains why stimulus intensity is commonly represented through temporal patterns and population activity rather than changes in single-spike shape or amplitude. For learners and practitioners, distinguishing graded local responses from all-or-none action potentials is essential for interpreting electrophysiology data, designing experiments, and understanding how the nervous system filters, amplifies, and transmits information under varying conditions.