Resting Potential: Function, Tasks, Role & Diseases

The resting potential is the voltage difference of -70 mV that exists between the interior and the surroundings of neurons in the nonexcited state. The potential is relevant to the formation of action potentials. Cyanide poisoning prevents restoration of the resting potential and leads to neuronal collapse.

What is the resting potential?

The resting potential is the voltage difference of -70 mV that exists between the interior and the surrounding area of neurons in the unexcited state. The resting potential is the voltage difference that exists between the interior of an unexcited neuron and its environment. This difference in voltage must be actively maintained and results from an unequal distribution of sodium and potassium ions. Two elements of the nerve cell membrane are involved in maintaining the resting potential: first, the sodiumpotassium pumps, and second, the ion channels on Ranvier’s laced rings. The resting potential of excitable neurons forms the basis for the saltatory conduction of excitation in human neural pathways. Upon excitation by an action potential, the cell is depolarized beyond its threshold potential and the voltage-gated ion channels open, causing a change in the resting potential with the influx of certain ions. The action potential is propagated down the neural pathways by the charge redistributions. The resting potential of a human neuron has a difference of -70 to -80 mV. The inside of the cell membrane is negatively charged and the outside is positively charged.

Function and task

Various processes occur at the cell membrane of an excitable cell during the resting phase. At Ranvier’s lacing rings, axons are not insulated with myelin. Na+/K+ pumps are located at these nodes, which transport potassium ions to the interior of the axon during the resting phase while consuming ATP. Sodium ions are pumped out of the cell at the same time. Thus, a higher concentration of potassium is present inside the axon than is present outside. The membranes of the cells have different permeability to these ions because of the proteinaceous ion channels. At rest, the sodium channels are generally closed. In contrast, the channels for potassium are open, so that diffusion of the potassium ions occurs. The ions thus diffuse outward. This occurs until there is a balance between the electrical forces and the osmotic pressure forces. This maintains a charge difference between the outside and inside of the cell membranes, also known as the resting potential. When a stimulus arrives on a nerve fiber and crosses the threshold, the voltage-dependent sodium and potassium channels open. This causes depolarization of the cell, which in turn triggers an action potential. The bioelectrical impulse is thus propagated along the nerve fibers. In simple terms, the action potential involves the transmission of a signal through changes in the membrane potential. A value of -50 mV is considered to be the threshold value for the development of an action potential. Thus, excitations below +20 mV do not give rise to an action potential and reactions fail to occur. After the formation and transmission of an action potential, the N+ channels close again first. The K+ channels, on the other hand, open to allow potassium ions to diffuse out of the axon. The electrical voltage inside the cell thus decreases again. This process is also called repolarization. Subsequently, the K+ channels also close and the potential of the cell drops below the resting potential. This hyperpolarization transitions to the resting potential, which is restored by the sodium-potassium pumps after about two milliseconds. The axon is thus ready for new action potentials.

Diseases and disorders

In phenomena such as cyanide poisoning, life-threatening consequences present themselves, sometimes due to the loss of the resting potential. Neurons require energy to restore resting potential. Cyanide poisoning blocks the supply of energy so that none can be provided for resting potential restoration. Thus, neurons remain permanently depolarized and lose functionality. Depending on how many neurons are affected by an undersupply of energy, the neuronal regulation of the entire organism can collapse in this way. Such a breakdown of neuronal regulation inevitably leads to death.In a broader sense, complaints with the resting potential of a neuron can also manifest themselves in ion channel diseases. These inherited diseases trigger excitation disorders in the musculature and nervous system. Ion channel diseases affect the switching behavior of ion channels. Changes in the switching behavior of the channels may in turn affect the resting potential recovery ability. Thus, the diseases affect the excitability of the tissue. In a narrower sense, ion channel diseases are mutations of the ion channels. Three forms of hereditary epilepsy are thought to be related to this phenomenon, according to scientific evidence. Hemiplegic migraine and idiopathic ventricular fibrillation are also explained in this way according to modern research. Sodium-potassium pumps can also be affected by diseases that have an impact on the resting potential of a nerve cell. According to many scientists, the modern Western diet provides an unnatural sodium-potassium ratio in the body. The excess of table salt and a lack of potassium due to too little plant food are said to be able to impair the sodium-potassium pumps, as the intracellular ion ratio can change in this way. Genetically determined disturbances of sodium-potassium exchange at the cell membrane, on the other hand, are present in some mutations and have been linked by researchers to forms of epilepsy, as have ion channel diseases. Thus, disturbances in resting potential restoration are probably relevant to various diseases of the central nervous system.