How Neurons Send Signals: Action Potentials and Synapses Explained

Every thought, memory and movement depends on cells called neurons passing signals to one another. Each neuron is a small biological machine that receives input, decides whether to fire and sends a message onward. The process is electrical inside the cell and chemical between cells. Understanding it explains a great deal of psychology, from how drugs change mood to how practice strengthens skills.

This guide walks through the parts of a neuron, how the electrical spike is generated, how signals cross the gap between cells and how these basics connect to behavior.

The parts of a neuron

A typical neuron has three main regions. The dendrites are branching extensions that receive input from other cells. The cell body, or soma, contains the nucleus and integrates the incoming signals. The axon is a long fiber that carries the outgoing message to other neurons, sometimes over distances of a meter or more in the human body.

At the far end of the axon are axon terminals. These terminals meet the dendrites or cell bodies of other neurons at junctions called synapses. The human brain is estimated to contain roughly 86 billion neurons, and each one can form thousands of synapses, which is why the total number of connections is so large.

The resting membrane potential

A neuron at rest is not inactive. Its membrane separates two fluids with different ion concentrations. Sodium ions are more concentrated outside the cell, and potassium ions are more concentrated inside. Pumps and channels keep this gradient in place, leaving the inside of the cell about 70 millivolts more negative than the outside. This difference is the resting membrane potential.

The gradient is a stored resource. Like water held behind a dam, it contains energy that can be released quickly when the membrane opens.

The action potential

When a neuron receives enough excitatory input, its membrane depolarizes, meaning the inside becomes less negative. If the voltage reaches a threshold of about negative 55 millivolts, voltage-gated sodium channels open. Sodium rushes in, the membrane swings strongly positive, and the neuron fires an action potential.

Within about a millisecond, potassium channels open and the membrane repolarizes. The cell then passes through a short refractory period in which it cannot fire again. These two features make the action potential an all-or-none event. A signal either reaches threshold and produces a full spike or it does not produce one at all.

Why spikes travel without fading

The action potential is regenerated at each patch of membrane along the axon. It does not weaken as it travels, which is how a signal can move the full length of a long axon intact. Myelin, a fatty insulating sheath wrapped around many axons, speeds this process by letting the signal jump between gaps called nodes of Ranvier. Myelinated fibers can carry signals at speeds above 100 meters per second, while thin unmyelinated fibers may be much slower.

Crossing the synapse

When an action potential reaches an axon terminal, it opens voltage-gated calcium channels. Calcium entering the terminal triggers small vesicles filled with neurotransmitter molecules to fuse with the membrane and release their contents into the gap, called the synaptic cleft.

The neurotransmitter diffuses across the cleft and binds to receptors on the receiving cell. Depending on the receptor, the effect is either excitatory, making the receiving neuron more likely to fire, or inhibitory, making it less likely. The chemical message is then cleared by reuptake into the sending cell, by enzymes that break it down or by diffusion away.

Common neurotransmitters

Several neurotransmitters are central to psychology. Glutamate is the main excitatory transmitter in the brain. GABA is the main inhibitory transmitter. Dopamine, serotonin and norepinephrine are sometimes called modulators because they change how strongly other circuits respond. Many psychiatric medications and recreational drugs act by changing how these chemicals are made, released, received or cleared.

Synaptic strength and learning

Synapses are not fixed. The strength of a connection can increase or decrease with use. The best-known example is long-term potentiation, a lasting increase in synaptic response after repeated stimulation. It was first described in the hippocampus in the 1970s and is widely studied as one cellular basis for learning and memory. The reverse process, long-term depression, weakens connections that are rarely used.

This plasticity explains why practice works. Repeated activation of a circuit makes its connections more efficient, so the same pattern of activity becomes easier to produce next time.

From cells to behavior

No single neuron represents a concept like a face or a word. Behavior emerges from large networks in which many neurons fire in patterns. A memory, for example, involves distributed activity across several regions rather than a single storage cell. Psychology studies the level of behavior and cognition, while neuroscience studies the cells and circuits. The two levels constrain each other.

Knowing the basics also helps separate real from exaggerated claims. The brain is not a simple switchboard with one area for each trait. Signals are graded, modulated and shaped by timing, and the same chemical can have different effects in different circuits.

A small table of signaling steps

The table below summarizes the main stages of signaling from one neuron to another. The timings are approximate and vary by cell type.

Stage	What happens	Rough timescale
Integration	Dendrites and soma sum incoming input	Milliseconds
Spike generation	Sodium influx and potassium efflux	About 1 millisecond
Conduction	Spike travels along the axon	Varies widely with myelination
Release	Calcium triggers vesicle fusion	Less than a millisecond
Receptor binding	Transmitter activates receptors	Sub-millisecond to milliseconds
Clearance	Transmitter is removed or broken down	Milliseconds to seconds

Why the signal stays one-way

A neuron's signal normally travels from the axon terminal to the next cell, not back the other way. Two features enforce this direction. The refractory period prevents the just-activated segment from firing again right away, and the release machinery sits only at the axon terminal, while receptors sit mainly on the receiving cell. The direction is not an absolute law of physics, since laboratory setups can trigger spikes in both directions, but in the living brain the arrangement keeps messages moving forward through a circuit.

Direction also matters for timing. Because each synapse adds a small delay for vesicle release and receptor binding, circuits with many synapses take measurable time to transmit information. This is one reason reaction times in psychology experiments are often tens to hundreds of milliseconds, even though a single action potential lasts only about a millisecond.

Glia and the support network

Neurons are not the only cells in the brain. Glial cells are roughly as numerous as neurons across the whole human brain, by estimates that vary widely across studies and regions, and they support neurons in several ways. Astrocytes help regulate the chemical environment around synapses and take up some released neurotransmitter. Oligodendrocytes produce the myelin that speeds conduction in the central nervous system. Microglia act as immune cells and help prune synapses during development.

Glia do not send spikes in the same way neurons do, but they shape how well neurons communicate. Changes in glial function are an active area of research in disorders such as multiple sclerosis, where myelin is damaged, and in studies of brain injury and development.

Key takeaways

Neurons communicate through electrical spikes inside the cell and chemical messages between cells. The action potential is an all-or-none event that is regenerated along the axon and does not fade with distance.

Synapses release neurotransmitters that excite or inhibit the next cell. Many psychiatric drugs and psychological effects act through these chemical messages.

Synapses change with experience, and this plasticity is one cellular basis of learning. Behavior arises from the patterns of activity across many neurons, not from single cells.