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Action Potential

An action potential is a brief, regenerative change in membrane voltage that transmits signals in electrically excitable cells.

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An action potential is a rapid, transient change in the voltage across a cell’s membrane, generated by coordinated changes in its permeability to ions. It is a principal signaling mechanism in neurons and also occurs in muscle and other electrically excitable cells. Unlike small, local voltage changes, an action potential can regenerate as it travels along an axon, allowing information to cross considerable distances without progressively losing its amplitude. Its electrical basis is the movement of ions through membrane channels, rather than electrons flowing through a metallic conductor. (openstax.org)

Ionic and electrical basis

The membrane potential is the electrical potential inside a cell relative to its exterior. At rest, many neurons have a resting membrane potential near −70 millivolts, although values vary among cell types. Sodium ions are generally more concentrated outside the cell, while potassium ions are more concentrated inside. Selective membrane permeability, particularly through potassium leak channels, contributes to the negative resting voltage. (openstax.org)

An ion’s movement depends on both its concentration difference and the electrical force acting on it: together these constitute an electrochemical gradient. The Nernst equation describes the equilibrium voltage for an individual ion. When channels open, the resulting ionic current tends to move the membrane potential toward that ion’s equilibrium potential. Ion channels are membrane proteins whose selectivity and gating determine which ions can cross and under what conditions. (ncbi.nlm.nih.gov)

The sodium–potassium pump uses ATP to maintain the sodium and potassium concentration differences. This sustained transport makes repeated electrical activity possible. The rapid voltage changes within an individual spike, however, arise chiefly from channel-mediated currents, not from the pump reversing each spike as it occurs. (ncbi.nlm.nih.gov)

Initiation andl segment, where voltage-gated sodium channels are densely concentrated. Inputs arriving through synapses produce graded potentials, which can combine to bring this region to its firing threshold. Threshold is the condition at which regenerative inward current becomes sufficient to drive a spike; it is not a universal voltage shared by all neurons. (openstax.org)

A typical sodium-dependent neuronal action potential has three overlapping phases:

  • Depolarization: Voltage-gated sodium channels activate rapidly. Sodium enters, making the membrane potential less negative and often positive. Depolarization opens additional channels, creating positive feedback.
  • Repolarization: Sodium channels inactivate while delayed voltage-gated potassium channels become more conductive. Outward potassium current returns the membrane voltage toward negative values.
  • Afterhyperpolarization: Potassium conductance may remain elevated briefly, taking the voltage below its resting level before it returns toward baseline. (nba.uth.tmc.edu)

Many neuronal spikes last roughly a millisecond, but duration and shape vary with channel composition and cellular conditions. The all-or-none principle means that, under comparable conditions, crossing threshold produces a full regenerative response rather than a spike proportional to stimulus strength. It does not mean that every cell has an identical waveform or that a neuron’s spikes can never change shape. (cvphysiology.com)

Refractory periods and information coding

During the absolute refractory period, sodium-channel inactivation prevents another ordinary sodium-dependent action potential from being generated. During the subsequent relative refractory period, some channels have recovered, but increased potassium conductance and incomplete sodium-channel recovery make firing more difficult. These processes constrain how rapidly a neuron can produce successive spikes. (openstax.org)

Because spike amplitude is relatively stereotyped, increasing stimulation is commonly represented by changes in firing frequency rather than proportionally larger spikes. The timing and patterns of spikes also distinguish neuronal responses. Thus, the all-or-none behavior of individual action potentials is compatible with varied signals carried by trains of spikes. (openstax.org)

Propagation along axons

An active membrane region produces local electrical currents that depolarize adjacent membrane. When the neighboring region reaches threshold, its channels generate another action potential. This successive regeneration distinguishes active propagation from passive voltage spread, which diminishes with distance. The signal does not require the same sodium ions to travel the entire length of the axon. (openstax.org)

In unmyelinated axons, regeneration occurs along successive membrane regions. In myelinated axons, myelin reduces current leakage and membrane capacitance, enabling local current to spread efficiently between nodes of Ranvier. Spikes are regenerated at these gaps, producing saltatory conduction. Conduction speed depends on axon diameter, myelination, and channel properties. (ncbi.nlm.nih.gov)

Synaptic output and muscle activity

At a chemical synapse, arrival of an action potential opens voltage-gated calcium channels in the presynaptic terminal. Calcium entry triggers synaptic vesicles to release neurotransmitters, converting the traveling electrical signal into chemical communication. The receiving cell’s response may increase or decrease its likelihood of firing. (openstax.org)

Muscle action potentials initiate excitation–contraction coupling. Cardiac waveforms differ markedly from typical neuronal spikes: ventricular muscle cells have a prolonged plateau supported by inward calcium current balanced against outward potassium current. Cardiac pacemaker cells instead undergo spontaneous depolarization between spikes, with calcium channels contributing to the upstroke. (ocw.mit.edu)

Experimental study

In 1952, Alan Hodgkin and Andrew Huxley published a quantitative account of excitation and conduction in the squid giant axon. Their Hodgkin–Huxley model represents membrane capacitance and voltage-dependent ionic conductances using differential equations. It reproduces spike generation from the measured behavior of sodium and potassium currents. (pmc.ncbi.nlm.nih.gov)

Patch-clamp experiments can resolve currents through individual channels. In current-clamp recordings, researchers measure voltage responses to injected current; voltage-clamp recordings instead control membrane voltage and measure the currents required to maintain it. These complementary approaches separate the whole-cell waveform from the channel mechanisms producing it. (ncbi.nlm.nih.gov)