Action potentials are the fundamental electrical signals that allow neurons to transmit information. These rapid changes in membrane voltage propagate along axons without losing strength. At rest, a neuron maintains a negative membrane potential of about negative 70 millivolts. This resting potential is established by the sodium-potassium pump and the different concentrations of ions across the membrane. There's a higher concentration of sodium ions outside the cell and more potassium ions inside.
An action potential has several distinct phases. It begins at the resting potential of negative 70 millivolts. When a stimulus causes the membrane to depolarize to the threshold potential of negative 55 millivolts, voltage-gated sodium channels rapidly open. This triggers the depolarization phase, where sodium ions rush into the cell, causing the membrane potential to rise sharply to positive 30 millivolts. Next, during repolarization, sodium channels inactivate while potassium channels open, allowing potassium to flow out of the cell. This restores the negative charge inside the membrane. The membrane potential briefly overshoots the resting potential during hyperpolarization, before finally returning to the resting state of negative 70 millivolts.
The action potential is controlled by voltage-gated ion channels in the cell membrane. At rest, most ion channels are closed, and the membrane potential is around negative 70 millivolts. When the membrane is depolarized to threshold, voltage-gated sodium channels rapidly open, allowing sodium ions to rush into the cell. This causes the sharp rise in membrane potential during the depolarization phase. The sodium channels quickly inactivate, and voltage-gated potassium channels open more slowly. Potassium ions flow out of the cell, causing repolarization. The delayed closing of potassium channels leads to the brief hyperpolarization before the membrane returns to its resting state. This precise choreography of ion channel opening and closing is what generates the characteristic shape of the action potential.
Action potentials propagate along axons without losing strength, allowing signals to travel long distances in the nervous system. When an action potential occurs at one location, local current flow depolarizes adjacent regions of the membrane to threshold, triggering new action potentials. This process continues along the axon, creating a wave of excitation. The refractory period, during which the membrane cannot generate another action potential, ensures that signals travel in one direction only. In myelinated axons, the myelin sheath acts as an insulator, and action potentials jump from one node of Ranvier to the next in a process called saltatory conduction. This significantly increases the speed of signal transmission, which is crucial for rapid neural communication.
Action potentials have significant clinical importance across many medical fields. Disruptions in action potential generation or propagation underlie numerous neurological disorders, including epilepsy, multiple sclerosis, and peripheral neuropathies. In the heart, abnormal action potentials can cause dangerous arrhythmias. Many medications target ion channels to modify action potentials. For example, local anesthetics block sodium channels to prevent pain signals from being transmitted. Antiarrhythmic drugs can target either sodium or potassium channels to regulate cardiac action potentials. Anticonvulsants often work by stabilizing neuronal membranes and preventing excessive action potential firing. Understanding the mechanisms of action potentials has led to the development of numerous therapeutic interventions that are essential in modern medicine.