Depolarization is the cancellation of charge differences on the two membrane sides of a nerve or muscle cell. The membrane potential changes to a less negative one as a result. In diseases such as epilepsy, the depolarization behavior of nerve cells changes.
What is depolarization?
Depolarization is the cancellation of charge differences on the two membrane sides of a nerve or muscle cell. Polarization exists between the two sides of an intact nerve cell membrane at rest, also known as membrane potential. Electrical poles form in the cell membrane as a result of charge separation. Depolarization is the loss of these properties as it occurs at the beginning of an excitation. Thus, during depolarization, the charge difference between the two sides of a biological membrane is momentarily cancelled. In neurology, depolarization is the change in membrane potential to positive or less negative values, as occurs when an action potential is passed. Reconstruction of the original polarization occurs toward the end of this process and is also referred to as repolarization. The opposite of depolarization is understood to be hyperpolarization, in which the voltage between the inside and outside of a biological membrane becomes even stronger, increasing beyond the voltage of the resting potential.
Function and task
The membranes of healthy cells are always polarized and thus exhibit a membrane potential. This membrane potential results from the difference in ion concentration on the two sides of the membrane. For example, ion pumps are located in the cell membrane of neurons. These pumps permanently produce an unequal distribution on the membrane surface, which differs from the charge on the inner side of the membrane. Intracellularly, there is thus an excess of negative ions and the cell membrane is more positively charged on the outside than on the inside. This results in a negative potential difference. The cell membrane of neurons has selective permeability and is thus differently permeable for different charges. Due to these properties, a neuron exhibits an electrical membrane potential. In the resting state, the membrane potential is called resting potential and is about -70 mV. Electrically conducting cells depolarize as soon as an action potential reaches them. The membrane charge is attenuated during depolarization as ion channels open. Ions flow into the membrane through the opened channels by diffusion, thus lowering the existing potential. For example, sodium ions flow into the nerve cell. This shift in charge balances the membrane potential and thus reverses the charge. Thus, in the broadest sense, the membrane is still polarized during an action potential, but in the opposite direction. In neurons, depolarization is either subthreshold or suprathreshold. The threshold corresponds to the threshold potential for ion channel opening. Normally, the threshold potential is about -50 mV. Larger values move the ion channels to open and trigger an action potential. Subliminal depolarization causes the membrane potential to return to the resting membrane potential and does not trigger an action potential. In addition to nerve cells, muscle cells are also capable of depolarization when an action potential reaches them. From central nerve fibers, excitation is transmitted to muscle fibers via the motor end plate. For this purpose, the end plate has cation channels that can conduct sodium, potassium and calcium ions. Sodium and calcium ion currents in particular flow through the channels due to their special driving forces, thereby depolarizing the muscle cell. In the muscle cell, the endplate potential rises from the resting membrane potential to the so-called generator potential. This is an electrotonic potential that, unlike the action potential, propagates passively across the membrane of the muscle fibers. If the generator potential is suprathreshold, an action potential is generated by the opening of the sodium channels and calcium ions flow in. Thus, muscle contraction occurs.
Diseases and disorders
In nervous system diseases such as epilepsy, the natural depolarization behavior of nerve cells changes. Hyperexcitability is the result. Epileptic seizures are characterized by abnormal discharge of neuronal associations that disrupt the normal activity of brain areas.With it, unusual perceptions and disturbances of motor function, thinking as well as consciousness occur. Focal epilepsy affects the limbic system or neocortex. Glutamatergic transmission triggers a high-amplitude excitatory postsynaptic potential in these areas. Thus, membraneigenic calcium channels are activated and undergo a particularly long-lasting depolarization. In this way, high-frequency bursts of action potentials characteristic of epilepsy are triggered. The abnormal activity spreads in an aggregate of several thousand neurons. Increased synaptic connectivity of neurons also contributes to the generation of the seizures. The same is true for abnormal intrinsic membrane properties, mainly involving ion channels. Synaptic transmission mechanisms are also often altered in the sense of receptor modifications. Persistent seizures are thought to result from synaptic looping systems that may involve larger brain areas. It is not only in epilepsy that the depolarization properties of neurons change. Numerous drugs also show effects on depolarization and manifest themselves either as hyperexcitability or hyperexcitability. These drugs include, for example, muscle relaxants, which cause complete relaxation of skeletal muscles by interfering with the central nervous system. Administration is common, for example, in spinal spasticity. Specifically, depolarizing muscle relaxants have an excitatory effect at the receptor of the muscles, initiating a long-lasting depolarization. Initially, the muscles do contract after drug administration, triggering uncoordinated muscle tremors, but shortly thereafter they cause flaccid paralysis of the respective muscles. As the depolarization of the muscles persists, the muscle is momentarily unexcitable.
