The threshold potential describes a specific charge difference at the membrane of excitable cells. When the membrane potential attenuates to a certain value in the course of depolarization, an action potential is induced via the opening of voltage-dependent ion channels. The value to be reached in each case, which is necessary for the generation of an action potential, is essential for excitation conduction because of the all-or-nothing principle.
What is the threshold potential?
The threshold potential describes a specific charge difference at the membrane of excitable cells. The cellular interior is separated from the surrounding external medium by a membrane that is only partially permeable to certain substances. Thus, ions, i.e. charged particles, cannot pass through it uncontrolled. The uneven distribution of ions between the inside and the outside of the cell causes a measurable electrochemical potential to build up, which is known as the threshold potential. As long as the cell is not excited, this resting membrane potential is negative. The electrical impulse arriving at the cell activates it or puts it into an excited state. The negative resting membrane potential is depolarized by a change in ion permeability, i.e. it becomes more positive. Whether a neuronal response occurs depends on the extent of this pre-depolarization. Only if a certain critical value is reached or exceeded, an action potential is formed according to the all-or-nothing principle. Otherwise, nothing happens. This specific value, necessary for excitation conduction by action potentials, is called the threshold potential.
Function and task
The point of contact for all incoming excitatory impulses is the axon hillock. This marks the site of action potential formation because the threshold potential is lower there than at other membrane sections due to a particularly high density of voltage-gated ion channels. As soon as the threshold potential is reached or exceeded in the course of pre-depolarization, a kind of chain reaction occurs. A large number of voltage-dependent sodium ion channels open abruptly. The temporary, avalanche-like sodium influx along the voltage gradient intensifies the depolarization until the resting membrane potential collapses completely. An action potential is established, i.e., for about one millisecond, a reversal of polarity occurs due to the excess of positive charges inside the cell. After an action potential has been successfully triggered, there is a gradual restoration of the original membrane potential. As the sodium influx slowly fails, delayed potassium channels open. The increasing potassium outward current compensates for the decreasing sodium inflow and counteracts 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 across the axon to the next nerve or muscle cell. The excitation conduction follows a constant mechanism. To compensate for depolarization, neighboring ions migrate to the site of formation of the action potential. This migration of ions also leads to a depolarization in the neighboring region, which induces a new action potential with a time delay when the threshold potential is reached. In markless nerve cells, continuous conduction of excitation along the membrane can be observed, whereas in nerve fibers sheathed by a myelin sheath, excitation jumps from cord ring to cord ring. The particular section of the membrane at which the action potential is initiated is unexcitable until the resting membrane potential is restored, which grants the conduction of excitation in only one direction.
Diseases and disorders
The threshold potential is the prerequisite for the generation of action potentials, on which all transmission of nerve impulses or excitation is ultimately based. Since excitation conduction is essential for all physiological functions, any disturbance of this sensitive electrophysiology can lead to physical limitations.Hypokalemia, i.e., potassium deficiency, has a delaying effect on depolarization and an accelerating effect on repolarization by weakening the resting membrane potential, which is associated with slowed conduction 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, resulting in an uncontrolled outflow of potassium ions from inside the cell and, consequently, the complete absence or weakening of the action potential. In addition, genetically determined mutations of the channel proteins for sodium and potassium can cause varying degrees of functional impairment, depending on the localization of the affected channels. For example, defects of the potassium channels in the inner ear are associated with sensorineural hearing loss. Pathologically altered sodium channels in skeletal muscles cause so-called myotonia, which is characterized by increased or prolonged tension and delayed relaxation of the muscles. This is caused by insufficient closure or blockage of the sodium channels, resulting in the generation of excessive action potentials. A disturbance 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 conduction chain may be disturbed: for example, the rhythm of automatic depolarization or the temporal coupling of depolarization of muscle cells or the frequency of excitation due to a lack of rest phases. As a rule, therapy is carried out with sodium channel blockers, which inhibit the sodium influx and thus stabilize the membrane potential on the one hand and delay the re-excitability of the cell on the other. In principle, all types of ion channels can be selectively blocked. In the case of voltage-dependent sodium channels, this is done by so-called local anesthetics. However, neurotoxins such as the venom of the mamba (dendrotoxin) or the venom of the puffer fish (tetrodotoxin) can also reduce or eliminate the excitability of the cell by inhibiting the sodium influx and preventing the generation of an action potential.
