Neurons transmit information through a combination of electrical signals within the cell and chemical signals between cells. A neuron generates a brief electrical impulse called an action potential, sends it racing down its length, then converts that electrical signal into a chemical message that crosses the tiny gap to the next neuron. This two-part system, electrical then chemical, is the foundation of everything your brain does.
The Starting Point: Resting Potential
Before a neuron can send a signal, it maintains a baseline electrical charge called the resting potential, sitting around -70 to -80 millivolts. That negative charge exists because the inside of the cell has a different mix of charged particles than the outside. Potassium is concentrated inside the cell (about 120 millimolar inside versus just 4 outside), while sodium is concentrated outside (140 millimolar outside versus 14 inside). The cell membrane is far more permeable to potassium than sodium at rest, so potassium slowly leaks out, leaving the interior slightly negative.
Maintaining this imbalance takes energy. A molecular pump constantly moves sodium out and potassium back in, and its activity accounts for an estimated 20 to 40 percent of the brain’s total energy consumption. The pump itself contributes very little to the voltage directly, but without it, the ion gradients would gradually collapse and neurons would lose the ability to fire.
How an Action Potential Fires
When a neuron receives enough stimulation, its membrane voltage rises toward a critical threshold. At that threshold, sodium channels in the membrane snap open, and sodium ions rush into the cell. This influx drives the voltage sharply positive in a spike called depolarization. The sodium channels open fast, within a fraction of a millisecond, creating a rapid, all-or-nothing electrical pulse.
Potassium channels have roughly the same activation threshold, but they open much more slowly. By the time potassium starts flowing out of the cell, sodium channels are already closing. The outward rush of potassium brings the voltage back down, a phase called repolarization, and briefly overshoots the resting potential before the cell settles back to baseline. The whole action potential lasts only about one to two milliseconds.
This pulse doesn’t fade over distance the way a sound fades in air. Instead, each patch of membrane regenerates the signal at full strength as it travels along the neuron’s axon, the long cable-like projection that carries signals away from the cell body.
Myelin Makes Signals Faster
Many axons are wrapped in myelin, a fatty insulating layer produced by specialized support cells. Myelin doesn’t cover the axon continuously. It leaves small exposed gaps called nodes of Ranvier spaced along the length. In an unmyelinated axon, the action potential has to be regenerated at every point along the membrane, which is slow. Myelin changes that. The insulation forces the electrical signal to jump rapidly through the interior of the axon from one node to the next, where sodium channels are concentrated and the signal gets a fresh boost.
This jumping pattern, called saltatory conduction, dramatically increases transmission speed. Signals in large myelinated axons can travel over 100 meters per second, compared to less than 1 meter per second in thin unmyelinated fibers. It also saves energy, because ion exchange only happens at the nodes rather than along the entire axon surface.
Crossing the Synapse
When the action potential reaches the end of the axon, it hits the synapse, the junction between one neuron and the next. Most synapses in the brain are chemical synapses, meaning the electrical signal gets converted into a chemical one to cross the gap.
Here’s the sequence: the arriving action potential opens calcium channels in the membrane of the sending neuron’s terminal. Calcium is roughly 10,000 times more concentrated outside the cell than inside, so it floods in rapidly. That calcium surge triggers tiny packets called vesicles, pre-loaded with neurotransmitter molecules, to fuse with the cell membrane and release their contents into the synaptic cleft, the narrow space between the two neurons. The released neurotransmitters then drift across the cleft and bind to receptors on the receiving neuron.
The entire process, from action potential arrival to neurotransmitter binding, takes roughly 0.5 to 1 millisecond. It’s fast, but not instantaneous, and that tiny delay adds up across the billions of synapses in the brain.
What Happens at the Receiving Neuron
Neurotransmitters don’t simply pass the signal along like a relay baton. They bind to receptors on the receiving neuron and either encourage or discourage it from firing. Some neurotransmitters open ion channels that let positive ions flow in, nudging the receiving cell’s voltage upward toward its firing threshold. These are excitatory signals. Others open channels that let negative ions in or positive ions out, pushing the voltage further from threshold. These are inhibitory signals.
A single neuron in the brain receives input from thousands of other neurons simultaneously. Each incoming signal produces a small, temporary voltage change. The neuron essentially adds them all up, both the excitatory pushes and the inhibitory pulls, in a process called summation. This integration happens in two ways: spatial summation, where signals arriving from different synapses at roughly the same time combine, and temporal summation, where rapid-fire signals from the same synapse stack on top of each other before the previous one fades.
If the combined total pushes the voltage past threshold at the base of the axon, the neuron fires its own action potential and passes the message forward. If inhibition wins, the neuron stays silent. This is how neurons make “decisions,” not through any one input, but through the balance of thousands of inputs at once.
Fast Receptors Versus Slow Receptors
Not all neurotransmitter receptors work the same way. Some are direct-gated ion channels: when the neurotransmitter binds, the channel opens immediately. These receptors produce effects within less than a millisecond and are responsible for the rapid, precise signaling that underlies moment-to-moment brain activity like processing a sound or moving a muscle.
Other receptors work indirectly. Instead of opening a channel themselves, they trigger a cascade of chemical events inside the cell that can modify ion channels, change gene expression, or adjust how sensitive the neuron is to future signals. These effects unfold over seconds to minutes, sometimes longer. This slower signaling handles things like mood regulation, learning, and long-term changes in how strongly two neurons are connected. Both types work in concert, with fast signaling carrying the immediate message and slow signaling tuning the system over time.
How the Signal Gets Cleared
Once a neurotransmitter has done its job, it needs to be removed from the synaptic cleft quickly. If it lingered, the receiving neuron would be stimulated (or inhibited) continuously, which would distort communication. Three main mechanisms handle cleanup. First, the neurotransmitter simply drifts away from the synapse through diffusion. Second, specialized transporter proteins on the sending neuron or nearby support cells actively pump the neurotransmitter back inside the cell for recycling, a process called reuptake. Third, enzymes in the cleft break certain neurotransmitters down into inactive fragments. Most synapses rely on a combination of these strategies.
Many psychiatric and neurological medications work by interfering with this clearance process. Slowing reuptake, for example, keeps the neurotransmitter active in the cleft for longer, amplifying its effects on the receiving neuron.
Electrical Synapses: The Fast Alternative
Not every synapse uses chemicals. A smaller number of synapses in the brain are electrical, connecting two neurons directly through tiny protein tunnels called gap junctions. These junctions are built from paired rings of proteins (called connexons) that line up precisely in both cell membranes, forming a continuous pore that lets ions flow straight from one neuron to the next.
The result is almost zero delay. A signal can cross an electrical synapse within a fraction of a millisecond, and much of that tiny delay is just the time it takes the action potential to reach the terminal, not the crossing itself. Electrical synapses are especially useful where speed and synchronization matter, like coordinating groups of neurons that need to fire in lockstep. The tradeoff is flexibility: electrical synapses can’t easily be strengthened, weakened, or switched from excitatory to inhibitory the way chemical synapses can.
Putting It All Together
The full chain of neural communication works like this: a neuron sits at its resting potential, receives thousands of excitatory and inhibitory inputs, sums them up, and fires an action potential if the total crosses threshold. That electrical impulse races down the axon (jumping between nodes if the axon is myelinated), triggers calcium-driven neurotransmitter release at the synapse, and the neurotransmitter binds to the next neuron’s receptors to start the process over again. The signal is then cleared from the cleft within milliseconds so the synapse is ready for the next round.
This cycle repeats billions of times per second across your nervous system. Every thought, sensation, memory, and movement emerges from neurons running through exactly this sequence, converting electricity to chemistry and back again, at extraordinary speed.