• [Wikipedia]: An action potential occurs when the membrane potential of a specific cell rapidly rises and falls. This depolarisation then causes adjacent locations to similarly depolarise. Action potentials occur in several types of animal cells, called excitable cells, which include neurons, muscle cells, and in some plant cells. Certain endocrine cells such as pancreatic beta cells, and certain cells of the anterior pituitary gland are also excitable cells.

In neurons, action potentials play a central role in cell-cell communication by providing for—or with regard to saltatory conduction, assisting—the propagation of signals along the neuron’s axon toward synaptic boutons situated at the ends of an axon; these signals can then connect with other neurons at synapses, or to motor cells or glands. In other types of cells, their main function is to activate intracellular processes. In muscle cells, for example, an action potential is the first step in the chain of events leading to contraction. In beta cells of the pancreas, they provoke release of insulin. Action potentials in neurons are also known as “nerve impulses” or “spikes”, and the temporal sequence of action potentials generated by a neuron is called its “spike train”. A neuron which emits an action potential, or nerve impulse, is often said to “fire”.

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In animal cells, there are two primary types of action potentials. One type is generated by voltage-gated sodium channels, the other by voltage-gated calcium channels. Sodium-based action potentials usually last for under one millisecond, but calcium-based action potentials may last for a hundred milliseconds or longer. In some types of neurons, slow calcium spikes provide the driving force for a long burst of rapidly emitted sodium spikes. In cardiac muscle cells, on the other hand, an initial fast sodium spike provides a “primer” to provoke the rapid onset of a calcium spike, which then produces muscle contraction.

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Nearly all cell membranes in animals, plants and fungi maintain a voltage difference between the exterior and interior of the cell, called the membrane potential. A typical voltage across an animal cell membrane is seventy millivolts. This means that the interior of the cell has a negative voltage relative to the exterior. In most types of cells, the membrane potential usually stays fairly constant. Some types of cells, however, are electrically active in the sense that their voltages fluctuate over time. In some types of electrically active cells, including neurons and muscle cells, the voltage fluctuations frequently take the form of a rapid upward (positive) spike followed by a rapid fall. These up-and-down cycles are known as action potentials. In some types of neurons, the entire up-and-down cycle takes place in a few thousandths of a second. In muscle cells, a typical action potential lasts about a fifth of a second. In plant cells, an action potential may last three seconds or more.

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All cells in animal body tissues are electrically polarised—in other words, they maintain a voltage difference across the cell’s plasma membrane, known as the membrane potential. This electrical polarisation results from a complex interplay between protein structures embedded in the membrane called ion pumps and ion channels. In neurons, the types of ion channels in the membrane usually vary across different parts of the cell, giving the dendrites, axon, and cell body different electrical properties. As a result, some parts of the membrane of a neuron may be excitable (capable of generating action potentials), whereas others are not. Recent studies have shown that the most excitable part of a neuron is the part after the axon hillock (the point where the axon leaves the cell body), which is called the axonal initial segment, but the axon and cell body are also excitable in most cases.

Each excitable patch of membrane has two important levels of membrane potential: the resting potential, which is the value the membrane potential maintains as long as nothing perturbs the cell, and a higher value called the threshold potential. At the axon hillock of a typical neuron, the resting potential is around seventy millivolts and the threshold potential is around fift-five millivolts. Synaptic inputs to a neuron cause the membrane to depolarise or hyperpolarise; that is, they cause the membrane potential to rise or fall. Action potentials are triggered when enough depolarisation accumulates to bring the membrane potential up to threshold.

When an action potential is triggered, the membrane potential abruptly shoots upward and then equally abruptly shoots back downward, often ending below the resting level, where it remains for some period of time. The shape of the action potential is stereotyped; this means that the rise and fall usually have approximately the same amplitude and time course for all action potentials in a given cell (exceptions are discussed later in the article). In most neurons, the entire process takes place in about a thousandth of a second. Many types of neurons emit action potentials constantly at rates of up to ten to a hundred per second. However, some types are much quieter, and may go for minutes or longer without emitting any action potentials.

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Several types of cells support an action potential, such as plant cells, muscle cells, and the specialised cells of the heart (in which occurs the cardiac action potential). However, the main excitable cell is the neuron, which also has the simplest mechanism for the action potential.

Neurons are electrically excitable cells composed, in general, of one or more dendrites, a single soma, a single axon and one or more axon terminals. Dendrites are cellular projections whose primary function is to receive synaptic signals. Their protrusions, known as dendritic spines, are designed to capture the neurotransmitters released by the presynaptic neuron.

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The amplitude of an action potential is often thought to be independent of the amount of current that produced it. In other words, larger currents do not create larger action potentials. Therefore, action potentials are said to be all-or-none signals, since either they occur fully or they do not occur at all. This is in contrast to receptor potentials, whose amplitudes are dependent on the intensity of a stimulus. In both cases, the frequency of action potentials is correlated with the intensity of a stimulus.

Despite the classical view of the action potential as a stereotyped, uniform signal having dominated the field of neuroscience for many decades, newer evidence does suggest that action potentials are more complex events indeed capable of transmitting information through not just their amplitude, but their duration and phase as well, sometimes even up to distances originally not thought to be possible.

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History: The role of electricity in the nervous systems of animals was first observed in dissected frogs by Luigi Galvani, who studied it from 1791 to 1797. His results inspired Alessandro Volta to develop the Voltaic pile—the earliest-known electric battery—with which he studied animal electricity (such as electric eels) and the physiological responses to applied direct-current voltages.

In the nineteenth century scientists studied the propagation of electrical signals in whole nerves (i.e., bundles of neurons) and demonstrated how nervous tissue was made up of cells, instead of an interconnected network of tubes (a reticulum). Carlo Matteucci followed up Galvani’s studies and demonstrated that injured nerves and muscles in frogs could produce direct current. His work inspired the German physiologist, Emil du Bois-Reymond, who discovered in 1843 that stimulating these muscle and nerve preparations produced a notable diminution in their resting currents, making him the first researcher to identify the electrical nature of the action potential.

The conduction velocity of action potentials was then measured in 1850 by du Bois-Reymond’s friend, Hermann von Helmholtz. Progress in electrophysiology stagnated thereafter due to the limitations of chemical theory and experimental practice.

To establish that nervous tissue is made up of discrete cells, the Spanish physician Santiago Ramón y Cajal and his students used a stain developed by Camillo Golgi to reveal the myriad shapes of neurons, which they rendered painstakingly. For their discoveries, they were both were awarded the 1906 Nobel Prize in Physiology. Their work resolved a long-standing controversy in the neuroanatomy of the nineteenth century; Camillo Golgi himself had argued for the network model of the nervous system.

The twentieth century saw significant breakthroughs in electrophysiology. In 1902 and again in 1912, Julius Bernstein advanced the hypothesis that the action potential resulted from a change in the permeability of the axonal membrane to ions. His hypothesis was confirmed by Ken Cole and Howard Curtis, who showed that membrane conductance increases during an action potential. In 1907, Louis Lapicque suggested that the action potential was generated as a threshold was crossed, what would be later shown as a product of the dynamical systems of ionic conductances.

In 1949, Alan Hodgkin and Bernard Katz refined Bernstein’s hypothesis by considering that the axonal membrane might have different permeabilities to different ions; in particular, they demonstrated the crucial role of the sodium permeability for the action potential. They made the first actual recording of the electrical changes across the neuronal membrane that mediate the action potential.

This line of research culminated in the five 1952 papers of Hodgkin, Katz and Andrew Huxley⁽*⁾, in which they applied the voltage clamp technique to determine the dependence of the axonal membrane’s permeabilities to sodium and potassium ions on voltage and time, from which they were able to reconstruct the action potential quantitatively. Hodgkin and Huxley correlated the properties of their mathematical model with discrete ion channels that could exist in several different states, including “open”, “closed”, and “inactivated”. Their hypotheses were confirmed in the mid-1970s and 1980s by Erwin Neher and Bert Sakmann, who developed the technique of patch clamping to examine the conductance states of individual ion channels.

> ⁽*⁾The study of action potentials has required the development of new experimental methods. The initial work, prior to 1955, was carried out primarily by Alan Lloyd Hodgkin and Andrew Fielding Huxley, who were, along John Carew Eccles, awarded the 1963 Nobel Prize in Physiology or Medicine for their contribution to the description of the ionic basis of nerve conduction. It focused on three goals: isolating signals from single neurons or axons, developing fast, sensitive electronics, and shrinking electrodes enough that the voltage inside a single cell could be recorded.

> The first problem was solved by studying the giant axons found in the neurons of the longfin inshore squid (Loligo forbesii and Doryteuthis pealeii, at the time classified as Loligo pealeii). These axons are so large in diameter (roughly one millimetre, or a hundred-fold larger than a typical neuron) that they can be seen with the naked eye, making them easy to extract and manipulate. However, they are not representative of all excitable cells, and numerous other systems with action potentials have been studied.
> The second problem was addressed with the crucial development of the voltage clamp, which permitted experimenters to study the ionic currents underlying an action potential in isolation, and eliminated a key source of electronic noise, the current associated with the capacitance of the membrane. Other electronic advances included the use of Faraday cages and electronics with high input impedance, so that the measurement itself did not affect the voltage being measured.

> The third problem, that of obtaining electrodes small enough to record voltages within a single axon without perturbing it, was solved in 1949 with the invention of the glass micropipette electrode, which was quickly adopted by other researchers. Refinements of this method are able to produce electrode tips that are as fine as a hundred angstrom, or ten nano-metres {an angstrom=one ten-millionth of a millimetre}, which also confers high input impedance. Action potentials may also be recorded with small metal electrodes placed just next to a neuron, with neurochips containing electrolyte-oxide-semiconductor field-effect transistors, or optically with dyes which are sensitive to the calcium status of an isolated cell, tissue or medium, or to voltage.

> While glass micropipette electrodes measure the sum of the currents passing through many ion channels, studying the electrical properties of a single ion channel became possible in the 1970s with the development of the patch clamp by Erwin Neher and Bert Sakmann. For this discovery, they were awarded the Nobel Prize in Physiology or Medicine in 1991. Patch-clamping verified that ionic channels have discrete states of conductance, such as open, closed and inactivated.

> Optical imaging technologies have been developed in recent years to measure action potentials, either via simultaneous multisite recordings or with ultra-spatial resolution. Using voltage-sensitive dyes, action potentials have been optically recorded from a tiny patch of cardiomyocyte membrane.

In the twenty-first century, researchers are beginning to understand the structural basis for these conductance states and for the selectivity of channels for their species of ion. Julius Bernstein was also the first to introduce the Nernst equation for resting potential across the membrane; this was generalised by David E. Goldman to the eponymous Goldman equation in 1943.

The sodium-potassium pump was identified in 1957 and its properties gradually elucidated, culminating in the determination of its structure by x-ray crystallography. The crystal structures of related ionic pumps have also been solved, giving a broader view of how these machines work. ~ (2012 Wikipedia Encyclopaedia).

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