Body processes

Threshold Potential – Function, Task & Diseases

Threshold potential

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 depolarization , an action potential is induced via the opening of voltage-gated ion channels. Due to the all-or-nothing principle, the value to be achieved in each case, which is necessary for the generation of an action potential, is essential for the excitation conduction .

What is the threshold potential?

The cellular interior is separated from the surrounding external medium by a membrane that is only partially permeable to certain substances. This means that ions, i.e. charged particles, cannot pass through them uncontrolled. The unequal distribution of ions between the inside and outside of the cell creates a measurable electrochemical potential 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 changed ion permeability, i.e. more positive. Whether a neuronal response occurs depends on the extent of this pre-depolarization. According to the all-or-nothing principle, an action potential is only generated when a certain critical value is reached or exceeded. Otherwise nothing happens. This specific value, necessary for the excitation conduction by means of action potentials, is called the threshold potential.

function & task

The contact point for all incoming excitation impulses is the axon hillock . This marks the place where the action potential is formed, since the threshold potential there is lower than in other sections of the membrane 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 influx of sodium along the voltage gradient amplifies the depolarization up to the complete collapse of the resting membrane potential. An action potential is built up, ie the polarity is reversed for about a millisecond due to the excess of positive charges inside the cell.

After an action potential has been successfully triggered, the original membrane potential is gradually restored. As the sodium influx slows down, delayed potassium channels open. The increasing potassium efflux 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 an action potential via the axon to the next nerve or muscle cell.

The conduction of excitation takes place with a constant mechanism. To compensate for the depolarization, neighboring ions migrate to the site of formation of the action potential. This migration of ions also leads to depolarization in the neighboring region, which induces a new action potential with a time delay when the threshold potential is reached.

In unmyelinated nerve cells, a continuous transmission of excitation along the membrane can be observed, whereas in nerve fibers that are surrounded by a myelin sheath , the excitation jumps from node to node. The part of the membrane where the action potential is triggered is not excitable until the resting membrane potential is restored, which allows the excitation to be transmitted in only one direction.

Diseases & Ailments

The threshold potential is the prerequisite for the development of action potentials, on which the entire transmission of nerve impulses or excitation is ultimately based. Because conduction is essential to all physiological functions, any disruption to this sensitive electrophysiology can result in physical disability. 

Hypokalemia, i.e. a lack of potassium , has the effect of delaying depolarization and accelerating 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 interior of the cell and thus the complete absence or weakening of the action potential.

In addition, genetically determined mutations in the channel proteins for sodium and potassium can cause functional impairments of varying severity, depending on the location of the affected channels. For example, defects in the potassium channels in the inner ear are associated with sensorineural hearing loss. Pathologically altered sodium channels in the skeletal muscles cause what are known as myotonia, which are characterized by increased or persistent muscle tension and delayed muscle relaxation . The reason for this is an insufficient closure or a 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 a 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 the lack of resting 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-gated sodium channels, this is done using so-called local anesthetics . But nerve toxins 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.

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Hello! I am Lisa Newlon, and I am a medical writer and researcher with over 10 years of experience in the healthcare industry. I have a Master’s degree in Medicine, and my deep understanding of medical terminology, practices, and procedures has made me a trusted source of information in the medical world.