An action potential is a short-term change in membrane potential. Action potentials typically arise at the axon hillock of a neuron and are the prerequisite for stimulus transmission.
What is the action potential?
Action potentials typically arise at the axon hillock of a nerve cell and are the prerequisite for stimulus transmissions. The action potential is a spontaneous reversal of charge in nerve cells. Action potentials arise at the axon hillock. The axon hillock is the point of origin of the transmitting processes of a nerve cell. The action potential then travels along the axon, or nerve projection. A potential can last from one millisecond to several minutes. The intensity of each action potential is the same. Accordingly, there are neither weak nor strong action potentials. They are rather all-or-nothing reactions, i.e. either a stimulus is strong enough to trigger an action potential completely or the action potential is not triggered at all. Each action potential proceeds in several phases.
Function and task
Before the action potential, the cell is in its resting state. The sodium channels are largely closed, and the potassium channels are partially open. By moving the potassium ions, the cell maintains the so-called resting membrane potential during this phase. This is about -70 mV. So if you would measure the voltage inside the axon, you would get a negative potential of -70 mV. This can be attributed to a charge imbalance of the ions between the space outside the cell and the cell fluid. The receptive processes of the nerve cells, the dendrites, receive stimuli and transmit them via the cell body to the axon hillock. Each incoming stimulus changes the resting membrane potential. However, for an action potential to be triggered, a threshold value must be exceeded at the axon hillock. Only when the membrane potential increases by 20 mV to -50 mV is this threshold reached. If the membrane potential only rises to -55 mV, for example, nothing happens due to the all-or-nothing response. Once the threshold is exceeded, the sodium channels of the cell open. Positively charged sodium ions flow in, and the resting potential continues to rise. The potassium channels close. The result is a repolarization. The space inside the axon is now positively charged for a short time. This phase is also called overshoot. Even before the maximum membrane potential is reached, the sodium channels close again. Instead, the potassium channels open and potassium ions flow out of the cell. Repolarization occurs, which means that the membrane potential approaches the resting potential again. For a short time, there is even a so-called hyperpolarization. During this process, the membrane potential still drops below -70 mV. This period, which lasts about two milliseconds, is also called the refractory period. During the refractory period, it is not possible to trigger an action potential. This is to prevent overexcitability of the cell. After regulation by the sodium-potassium pump, the voltage is again at -70 mV and the axon can again be excited by a stimulus. The action potential is now transmitted from one section of the axon to the next. Because the previous section is still in the refractory period, stimulus transmission can only occur in one direction at a time. However, this continuous stimulus transmission is rather slow. Saltatory stimulus transmission is faster. Here, the axons are surrounded by a so-called myelin sheath. This acts like a kind of insulation band. In between, the myelin sheath is repeatedly interrupted. These interruptions are called lacings. During saltatory stimulus transmission, the action potentials jump from one cord ring to the next. This greatly increases the rate of propagation. The action potential is the basis of the transmission of stimulus information. All functions of the body are based on this conduction.
Diseases and disorders
When the myelin sheaths of nerve cells are attacked and destroyed, there are serious disturbances in the transmission of stimuli. The loss of the myelin sheath causes charge to be lost during conduction. This means that more charge is needed to excite the axon at the next break in the myelin sheath.In the case of slight damage to the myelin layer, the action potential is delayed. If there is severe damage, excitation conduction may be completely interrupted, as no action potential can be triggered anymore. Myelin sheaths can be affected by genetic defects such as Krabbe disease or Charcot-Marie-Tooth disease. However, the best known demyelinating disease is probably multiple sclerosis. Here, the myelin sheaths are attacked and destroyed by the body’s own immune cells. Depending on which nerves are affected, visual disturbances, general weakness, spasticity, paralysis, sensitivity or speech disorders may occur. A rather rare disease is paramyotonia congenita. On average, only one person is affected out of every 250,000 people. The disease is a disorder of the sodium channel. As a result, sodium ions can enter the cell even in phases when the sodium channel should actually be closed, thus triggering an action potential even if there is actually no stimulus at all. Consequently, there can be a permanent tension in the nerves. This manifests itself as increased muscle tension (myotonia). After a voluntary movement, the muscles slacken with a significant delay. The reverse is also conceivable in paramyotonia congenita. It may be that the sodium channel does not allow sodium ions into the cell even during excitation. Thus, an action potential may be triggered only with a delay or not at all despite an incoming stimulus. The reaction to the stimulus thus fails to occur. The consequences are sensory disturbances, muscle weakness or paralysis. The occurrence of symptoms is particularly favored by low temperatures, which is why those affected should avoid any cooling of the muscles.
