The Threshold potential describes a specific charge difference on the membrane of excitable cells. If the membrane potential weakens to a certain value in the course of the depolarization, an action potential is induced via the opening of voltage-dependent ion channels. The value to be achieved in each case, which is necessary for the generation of an action potential, is essential for the conduction of excitation due to the all-or-nothing principle.
What is the threshold potential?
The cellular interior is separated from the surrounding external medium by a membrane, which is only partially permeable to certain substances. This means that ions, i.e. charged particles, cannot pass through them in an uncontrolled manner. Due to the uneven distribution of the ions between the inside and the outside of the cell, a measurable electrochemical potential builds up, which is referred to as the threshold potential.
As long as the cell is not stimulated, this resting membrane potential is negative. The electrical impulse arriving at the cell activates it or puts it in an excited state. The negative resting membrane potential is depolarized by a changed ion permeability, i.e. more positive. Whether a neural response occurs depends on the extent of this pre-depolarization. According to the all-or-nothing principle, an action potential is only created when a certain critical value is reached or exceeded. Otherwise nothing happens. This specific value necessary for the conduction of excitation by means of action potentials is referred to as the threshold potential.
Function & task
The point of contact for all incoming excitation impulses is the axon mound. This marks the place where the action potential is formed, since the threshold potential is lower there than on other membrane sections due to a particularly high density of voltage-dependent ion channels.
As soon as the threshold potential is reached or exceeded in the course of the pre-depolarization, a kind of chain reaction occurs. A large number of voltage-dependent sodium ion channels suddenly open. The temporary, avalanche-like sodium influx along the voltage gradient intensifies the depolarization up to the complete collapse of the resting membrane potential. An action potential is established, i.e.for about a millisecond, the excess positive charges inside the cell cause a reversal of polarity.
After an action potential has been successfully triggered, the original membrane potential is gradually restored. While the sodium influx is slow, delayed potassium channels open. The increasing potassium outflow compensates for the decreasing sodium influx and counteracts the depolarization. In the course of this so-called repolarization, the membrane potential becomes negative again and even briefly falls below the value of the resting potential.
The sodium-potassium pump then restores the original ion distribution. The excitation spreads in the form of the action potential via the axon to the next nerve or muscle cell.
The excitation conduction takes place in a constant mechanism. To compensate for the depolarization, neighboring ions migrate to the place where the action potential is formed. This migration of ions also leads to a depolarization in the neighboring region, which induces a new action potential with a delay when the threshold potential is reached.
In the case of non-medullary nerve cells, a continuous transmission of excitation along the membrane can be observed, whereas in nerve fibers that are covered by a myelin sheath, the excitation jumps from ring to ring. The respective section of the membrane at which the action potential is triggered cannot be excited until the resting membrane potential is restored, which allows the excitation to be passed on in only one direction.
Illnesses & ailments
The threshold potential is the prerequisite for the creation of action potentials, on which ultimately the entire transmission of nerve impulses or excitation is based. Since the conduction of excitation is essential for all physiological functions, any disturbance of this sensitive electrophysiology can lead to physical limitations.
Hypokalaemia, i.e. a potassium deficiency, has a slowing effect on the depolarization and accelerates the repolarization by weakening the resting membrane potential, which is associated with slower conduction of excitation and the risk of muscle weakness or paralysis. In diseases that damage the myelin sheath of nerve fibers (e.g. multiple sclerosis), the underlying potassium channels are exposed, which results in an uncontrolled outflow of potassium ions from the inside of the cell and thus the complete absence or weakening of the action potential.
In addition, genetic mutations in the channel proteins for sodium and potassium can cause functional impairments of varying degrees, depending on the location of the affected channels. For example, defects in the potassium channels in the inner ear are associated with inner ear hearing loss. Pathologically altered sodium channels in the skeletal muscles cause so-called myotonia, which are characterized by increased or sustained tension and delayed relaxation of the muscles. The reason for this is an insufficient closure or blockage of the sodium channels and thus the generation of excessive action potentials.
A disruption of the sodium or potassium channels in the heart muscles can trigger arrhythmias, i.e. cardiac arrhythmias such as an increased heart rate (tachycardia), since only the proper conduction of excitation in the heart guarantees a steady, independent heart rhythm. In the case of tachycardia, different elements within the transmission chain can be disturbed: for example the rhythm of the automatic depolarization or the temporal coupling of the depolarization of muscle cells or the frequency of excitation due to lack of rest phases.
As a rule, therapy is carried out with sodium channel blockers, which inhibit the sodium influx and thus on the one hand stabilize the membrane potential and on the other hand delay the re-excitability of the cell. In principle, all types of ion channels can be selectively blocked. In the case of voltage-dependent sodium channels, this is done via so-called local anesthetics. But neurotoxins such as the poison of the mamba (dendrotoxin) or the poison of the puffer fish (tetrodotoxin) can reduce or switch off the excitability of the cell by inhibiting the influx of sodium and preventing the development of an action potential.
