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When a biological cell or patch of membrane undergoes an action potential, the polarity of the transmembrane voltage swings rapidly from negative to positive and back. A cell capable of undergoing an action potential is said to be excitable. Within any one excitable cell, consecutive action potentials typically are indistinguishable. Also between different cells the amplitudes of the voltage swings tend to be roughly the same. But the speed and simplicity of action potentials vary significantly between cells, in particular between different cell types.
Minimally, an action potential involves a depolarization, a repolarization and finally a hyperpolarization (or "undershoot"). In specialized muscle cells of the heart, such as the pacemaker cells, a "plateau phase" of intermediate voltage may precede repolarization.
The transmembrane voltage changes that take place during an action potential result from changes in the permeability of the membrane to specific ions, the internal and external concentrations of which are in imbalance. In the axon fibers of nerves, depolarization results from the inward rush of sodium ions, while repolarization and hyperpolarization arise from an outward rush of potassium ions. Calcium ions make up most or all of the depolarizing currents at an axon's pre-synaptic terminus, in muscle cells and in some dendrites.
Changes in membrane permeability and the onset and cessation of ionic currents reflect the opening and closing of "voltage-gated" ion channels, which provide portals through the membrane for ions. Residing in and spanning the membrane, these enzymes sense and respond to changes in transmembrane potential.
Action potentials are triggered by an initial depolarization to the point of threshold. This threshold potential varies but generally is about 15 millivolts above the resting potential of the cell. Typically action potential initiation occurs at a synapse, but may occur anywhere along the axon. In his discovery of "animal electricity," Luigi Galvani elicited an action potential through contact of his scalpel with the motor nerve of a frog he was dissecting, causing one of its legs to kick as in life.
The propagation speed of these "impulses" is faster in fatter fibers than in thin ones, other things being equal. In their Nobel prize-winning work uncovering the wave nature and ionic mechanism of action potentials, Alan Hodgkin and Andrew Huxley performed experiments on the "giant fiber" of Atlantic squid[?]. Responsible for initiating flight, this axon is fat enough to be seen without a microscope (100 to 1000 times larger than is typical). This is assumed to reflect an adaptation for speed. Indeed, the velocity of nerve impulses in these fibers is among the fastest in nature.
Many neurons have insulating sheaths of "myelin" surrounding their axons, which enable action potentials to travel faster than in unmyelinated axons of the same diameter. The myelin sheathing normally runs along the axon in sections about 1 mm long, punctuated by unsheathed nodes of Ranvier.
Because the salty cytoplasm of the axon is electrically conductive, and because the myelin inhibits charge leakage through the membrane, depolarization at one node is sufficient to elevate the voltage at a neighboring node to the threshold for action potential initiation. Thus in myelinated axons, action potentials do not propagate as waves, but recur at successive nodes and in effect hop along the axon. This mode of propagation is known as saltatory conduction.
The disease multiple sclerosis (MS) is due to a breakdown of myelin sheathing, and degrades muscle control by destroying axons' ability to conduct action potentials.
Action potentials are measured with the recording techniques of electrophysiology. In the case of an archetypal nerve action potential on an oscilloscope, the relatively large swing to a more positive value, followed by the repolarization recovery and undershoot together trace an arc that could be described as a distorted sine wave--or like the blips on hospital EKG machines that can be seen on TV (these EKG waves are a smear of all the action potentials in one heartbeat, so they enact more slowly than any individual "A.P." and have a somewhat more complicated shape). In an unmyelinated axon that is "firing" an action potential, the transmembrane potential at any instant will vary from point to point along the fiber, with its amplitude depending on whether the A.P. wave has reached that point or passed it, and how long ago. A recording from a single point will show the various stages of the action potential enacted--depolarization, repolarization, hyperpolarization--as the wave passes.
Depolarization and repolarization together are complete in about two milliseconds, while undershoots can last hundreds of milliseconds, depending on the cell. In neurons, the exact length of the roughly two-millisecond delay in repolarization can have a strong effect on the amount of neurotransmitter released at a synapse. The duration of the hyperpolarization determines a nerve's "refractory period" (how long until it may conduct another action potential) and hence the frequency at which it will fire under continuous stimulation. Both of these properties are subject to biological regulation, primarily (among the mechanisms discovered so far) acting on ion channels selective for potassium.