활동전위

Neurons typically maintain a resting membrane potential of approximately negative 70 millivolts. This electrical difference across the cell membrane is maintained by the sodium-potassium pump, which establishes higher sodium concentrations outside the cell and higher potassium concentrations inside. This resting state is the baseline from which action potentials are triggered.

When a neuron depolarizes to threshold, voltage-gated sodium channels open first, allowing sodium to rush inward down its electrochemical gradient, rapidly raising membrane potential to about positive 40 millivolts. Sodium channels then inactivate while voltage-gated potassium channels open more slowly, allowing potassium to flow outward, repolarizing the membrane. This sequential channel activity creates the characteristic spike of an action potential.

The refractory period is a brief interval after an action potential when the membrane becomes hyperpolarized, making it nearly impossible for a new action potential to fire. This period prevents the action potential from traveling backward along the axon and ensures unidirectional signal propagation. It also limits the maximum frequency at which neurons can generate successive action potentials.

Myelin wrapping from oligodendrocytes and Schwann cells insulates axons, preventing current leakage. Voltage-gated channels concentrate at nodes of Ranvier, gaps between myelin segments. The action potential regenerates at each node through saltatory conduction, allowing the signal to jump rapidly along the axon rather than propagating continuously, dramatically increasing conduction velocity.

Depolarization occurs when the membrane potential becomes less negative, typically when sodium ions flow inward through open channels. Hyperpolarization occurs when the membrane potential becomes more negative, usually from potassium efflux or inhibitory signals. Both changes alter the likelihood of reaching threshold and triggering an action potential, allowing neurons to integrate incoming signals.

Squid axons are much larger than mammalian neurons, enabling faster action potentials needed for rapid escape responses. Their larger diameter made them ideal for electrode recordings and experimental manipulation. In the 1950s, Alan Hodgkin and Andrew Huxley used squid giant nerves to pioneer quantitative descriptions of sodium and potassium permeability, establishing the ionic basis of action potentials.

Action potentials propagate as all-or-none electrical signals along axons, triggering neurotransmitter release at axon terminals. These neurotransmitters bind to receptors on receiving neurons, transmitting information across synapses. The rapid, stereotyped nature of action potentials allows reliable signal transmission throughout the nervous system, enabling communication between neurons and coordination of body functions.