In physiology, an action potential is a short, rapid raise and then fall of the the electrical membrane potential.
A resting excitable cell is negatively charged with relate to its environment (see reversal potential). In addition, it must be at least two ions that have different concentration in the cell than outside (K+ and Na+, for instance).
Voltage gated channels are closed when the membrane potential is near the resting potential of the cell, open when the membrane potential decreases (approaches zero)[1] below a precisely defined threshold value. Typically the electric potential inside membrane pushes some part of the gated channel (voltage sensor) that opens the channel like rotating handle opens the tap. Ions start to cross the membrane in the direction of the electrochemical gradient[2], further pushing the potential toward positive that opens even more channels. This proceeds explosively until all of the available ion channels are open, resulting in a large upswing in the membrane potential.
Close to zero and positive membrane potential opens the second group of voltage gated channels, specific to the different ion (usually K+), that has the electrochemical gradient opposite to the ion that caused the initial excitation. These second stage currents are strong enough to overcome the effect of excitation, returning the potential back to the resting state and closing the channels of the first group (by moving they voltage sensor back to the "closed" position). After the second, "restoring" group also closes, the cell is ready to generate one more action potential. The single action potential does not significantly change the concentration if ions inside and outside the cell. Only after tens or even hundreds of excitations the cell needs its ion pumps to restore the concentrations using the energy of ATP.
Neuron uses Na+ channels to generate the potential and K+ channels to restore the negative resting potential. The action potential is a response to some events that increase it (make less negative), often as result of the signal from other neurons. The cell normally has more K+ and less Na+ inside than in the surrounding environment.
For small voltage increases from rest, the K+ current exceeds the Na+ current and the voltage returns to its normal resting value. However, if the voltage increases past a critical threshold (often 15 mV over the resting value), the Na+ current still dominates and the chain reaction starts. The positive feedback from the sodium current activates even more sodium channels. Thus, the cell "fires" again, producing a sequence of spikes action potential.
Currents produced by the opening of the voltage-gated channels are much stronger than the initial stimulating current. Hence amplitude, shape and duration of the action potential are mostly determined by the properties of these channels and not the duration or amplitude of the stimulus. However neurons are capable to "represent" the strength of the excitation by varying the time interval between the subsequent spikes.
Only small percent of ions need to cross the membrane to generate the action potential.
Same as neural cells, a given cardiac myocyte has a negative resting potential.
A notable difference between skeletal and cardiac myocytes is how each elevates the Ca2+ to induce contraction. When skeletal muscle is stimulated to contract, influx of Na+ quickly depolarizes the skeletal myocyte and triggers calcium release from the endoplasmic reticulum (called sarcoplasmic reticulum for myocyte cells). In cardiac myocytes, the release of Ca2+ from the sarcoplasmic reticulum is induced by Ca2+ influx into the cell through voltage-gated calcium channels on the outer cell membrane. This phenomenon is called calcium-induced calcium release and increases the myoplasmic free Ca2+ concentration causing muscle contraction. In both muscle types, after a delay (the absolute refractory period), potassium channels reopen and the resulting flow of K+ out of the cell causes repolarization to the resting state. The voltage-gated calcium channels in the cardiac sarcolemma are generally triggered by an influx in sodium during the "0" phase of the action potential.
In addition to stimulus from adjacent cells, certain cells of the heart have the ability to undergo spontaneous depolarization, in which an action potential is generated without influence from nearby cells. This allows the heart to work without any external stimuli and is known as cardiac muscle automaticity.
A notable difference between skeletal and cardiac myocytes is how each elevates the Ca2+ to induce contraction. When skeletal muscle is stimulated to contract, influx of Na+ quickly depolarizes the skeletal myocyte and triggers calcium release from the endoplasmic reticulum (called sarcoplasmic reticulum for myocyte cells). In cardiac myocytes, the release of Ca2+ from the sarcoplasmic reticulum is induced by Ca2+ influx into the cell through voltage-gated calcium channels on the outer cell membrane. This phenomenon is called calcium-induced calcium release. In both muscle types, after a delay (the refractory period), K+ channels reopen and the resulting flow of K+ out of the cell returns the membrane potential to the resting state.
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