The nervous system acts as the body’s rapid communication network, allowing us to perceive the world and react instantly. This communication relies on a specialized electrical message called a nerve impulse, which travels along nerve cells, or neurons. This message transfer enables everything from muscle contraction to complex thought processes.
Establishing the Resting Potential
Before a neuron transmits a message, it maintains a steady, polarized state known as the resting membrane potential. In this state, the inside of the neuron is electrically negative compared to the fluid surrounding the cell. This difference, typically around -70 millivolts, is established by an unequal distribution of charged particles, or ions, across the cell membrane.
The primary players in maintaining this charge difference are sodium (Na+) and potassium (K+) ions. The concentration of Na+ is higher outside the neuron, while the concentration of K+ is higher inside. Additionally, large, negatively charged protein anions are trapped within the cell, contributing to the internal negativity of the resting potential.
To maintain this necessary imbalance, the neuron utilizes the Sodium-Potassium Pump (Na+/K+ ATPase). This pump uses energy derived from ATP to exchange ions across the membrane. It expels three Na+ ions out of the cell for every two K+ ions it brings in, which contributes to keeping the interior more negative.
The membrane possesses specialized potassium leakage channels that allow some K+ to slowly diffuse out of the cell down its concentration gradient. These leakage channels, combined with the continuous action of the Na+/K+ pump, work together to establish and stabilize the resting potential.
The Generation of the Action Potential
The resting state is interrupted when the neuron receives a stimulus strong enough to trigger an action potential. This signal requires reaching a specific voltage level, known as the threshold stimulus, before the impulse can fire. If the stimulus is too weak, the cell returns to rest, but if the threshold is met, the process proceeds completely in an “all-or-none” manner.
The initial event is the opening of voltage-gated sodium channels embedded in the membrane. Once the threshold is crossed, these channels snap open, allowing a massive influx of Na+ ions into the neuron. This movement of positive charge causes the membrane potential to flip from negative to positive, a process called depolarization.
As the membrane potential peaks, reaching about +30 millivolts, the sodium channels inactivate and close, preventing further Na+ entry. Almost simultaneously, the voltage-gated potassium channels open in response to the positive internal charge. K+ ions then rush out of the cell, driven by both their concentration and electrical gradients.
This efflux of K+ ions works to restore the original negative charge inside the cell, a phase known as repolarization. Because the potassium channels are slow to close, they often allow slightly more K+ to leave than is necessary, causing a brief period of excessive negativity called hyperpolarization, or the undershoot.
Following hyperpolarization, the voltage-gated channels return to their closed, resting state, and the Na+/K+ pump works to re-establish the precise ion concentrations. The entire action potential sequence, from threshold to hyperpolarization, occurs in just a few milliseconds.
Signal Movement Along the Axon
Once an action potential is generated at the beginning of the axon, the signal must propagate efficiently down the entire length of the nerve fiber. The influx of sodium ions during depolarization creates a localized positive charge that then acts as a stimulus for the adjacent section of the axon membrane. This sequential depolarization ensures the impulse moves forward without losing strength.
The speed of this transmission is enhanced in many neurons by a fatty, insulating layer called the myelin sheath, which is formed by specialized glial cells. This myelin wraps tightly around the axon, preventing ion leakage and acting as an electrical insulator. The action potential cannot occur in the myelinated segments because there are no voltage-gated channels present under the sheath.
Instead, the impulse effectively “jumps” from one gap in the myelin to the next, a process called saltatory conduction. These regularly spaced gaps, where the axon membrane is exposed, are known as the Nodes of Ranvier. Voltage-gated channels are highly concentrated only at these nodes.
When the impulse arrives at a Node of Ranvier, a new, full-strength action potential is generated, which then travels passively and extremely quickly under the myelin to the next node. This saltatory mechanism increases the speed of transmission by up to 100 times compared to continuous conduction, where the signal must be regenerated point-by-point along an unmyelinated axon. This efficiency is why motor neurons, which require quick responses, are often myelinated.
Chemical Communication at the Synapse
The electrical signal, having traveled the length of the axon, typically cannot jump directly to the next cell and must transition into a chemical message. This transfer occurs at the synapse, a specialized junction between the transmitting neuron (presynaptic cell) and the receiving cell (postsynaptic cell). The tiny physical gap between the two cells is called the synaptic cleft.
When the action potential reaches the very end of the presynaptic axon terminal, it triggers the opening of voltage-gated calcium (Ca++) channels. Calcium ions, which are highly concentrated outside the cell, rush into the terminal in response to this electrical change. This influx of Ca++ is the immediate trigger for the next step in communication.
The rise in internal calcium concentration causes small, membrane-bound sacs, known as synaptic vesicles, to fuse with the presynaptic membrane. These vesicles contain chemical messengers called neurotransmitters, which are then released into the synaptic cleft through a process called exocytosis. These molecules rapidly diffuse across the narrow gap to the postsynaptic side.
Once in the cleft, the neurotransmitters bind to specific receptor proteins located on the membrane of the postsynaptic cell. This binding causes ion channels on the receiving cell to open or close. Depending on the specific neurotransmitter and receptor, the result can be either an excitatory effect, making the postsynaptic neuron more likely to fire its own action potential, or an inhibitory effect, making it less likely to fire.
This chemical signaling is brief and regulated to ensure precision and prevent constant stimulation. The neurotransmitters must be quickly removed from the cleft either by enzymatic breakdown or reuptake into the presynaptic terminal. This rapid cleanup ensures the synapse is prepared for the arrival of the next nerve impulse, thereby completing the cycle of neural communication.