Aktionspotential

A neuron's resting membrane potential is approximately -70 millivolts, maintained by the unequal distribution of ions across the cell membrane. This negative charge can be altered by signals such as neurotransmitters or sensory stimuli, causing the membrane to either depolarize (become more positive) or hyperpolarize (become more negative).

When the membrane potential depolarizes to threshold, voltage-gated sodium channels open, allowing sodium ions to rush into the cell down their electrochemical gradient. This positive ion influx further depolarizes the membrane, opening more sodium channels in a positive feedback loop that rapidly raises the membrane potential to approximately +30 to +40 millivolts.

During repolarization, sodium channels inactivate while voltage-gated potassium channels open more slowly. Potassium ions then flow out of the cell down their concentration gradient, removing positive charge. The reduced sodium influx combined with potassium efflux rapidly lowers the membrane potential back toward resting levels.

The refractory period is a brief interval after an action potential when the membrane potential dips below resting potential, making the cell incapable of producing another action potential. This hyperpolarization prevents the action potential from moving backward along the axon, ensuring unidirectional signal propagation through the nervous system.

Myelin sheath, formed by oligodendrocytes in the central nervous system and Schwann cells in the peripheral nervous system, insulates axons and prevents current leakage. Voltage-gated channels are concentrated at nodes of Ranvier between myelin segments, allowing the action potential to jump between nodes in a process called saltatory conduction, dramatically increasing propagation speed.

Giant squid axons are much larger in diameter than mammalian neurons, enabling faster action potentials necessary for rapid escape maneuvers. Their size allowed researchers like Hodgkin and Huxley in the 1950s to insert electrodes and directly measure ionic currents, providing the first quantitative descriptions of sodium and potassium permeability during action potentials.

Neurotransmitters released at axon terminals bind to receptors on the receiving neuron, triggering changes in membrane potential through excitatory and inhibitory effects. Excitatory signals depolarize the membrane toward threshold, while inhibitory signals hyperpolarize it, together determining whether an action potential will be generated.