A synapse is the tiny junction where one nerve cell passes a signal to another. Your brain contains roughly 164 trillion of these connections in the outer layer alone, and every thought, movement, memory, and sensation depends on signals crossing them. The gap between the two cells at a synapse is astonishingly small, typically 15 to 25 nanometers, far too thin to see without an electron microscope.
How a Synapse Is Built
A synapse has three main parts. The sending side, called the presynaptic terminal, sits at the tip of one nerve cell’s long fiber. This terminal is packed with tiny bubble-like sacs filled with chemical messengers. The receiving side, called the postsynaptic membrane, belongs to the next cell and is loaded with receptor proteins designed to detect those messengers. Between the two sits the synaptic cleft, a narrow fluid-filled gap where the chemical handoff takes place.
Supporting cells called astrocytes also wrap around many synapses. Their job includes mopping up leftover chemical messengers after a signal has been sent, keeping background levels low so the next signal comes through clearly. Because astrocytes play such an active role, scientists sometimes refer to the setup as a “tripartite synapse,” a three-part partnership between the sending cell, receiving cell, and its astrocyte neighbor.
How Signals Cross the Gap
When an electrical impulse races down a nerve cell and reaches the presynaptic terminal, it triggers a chain of events that converts that electrical signal into a chemical one. Calcium rushes in through specialized channels in the membrane, and that calcium influx causes the messenger-filled sacs to merge with the cell wall and spill their contents into the cleft. A single sac can hold anywhere from about 1,000 to 50,000 molecules of a chemical messenger. Only about 10% of the available sacs release their contents at any given moment, leaving the rest in reserve.
Once released, the messenger molecules diffuse across the gap in microseconds and lock onto receptors on the receiving cell. That binding either excites the next cell, pushing it closer to firing its own electrical impulse, or inhibits it, making it less likely to fire. The whole crossing introduces a brief delay of 0.5 to 4 milliseconds, which is why chains of many synapses can slow a signal noticeably compared to a direct electrical connection.
Excitatory vs. Inhibitory Signals
Not all synaptic signals do the same thing. Excitatory messengers, like glutamate (the most common one in the brain), open channels that let positively charged particles flood into the receiving cell. This shifts the cell’s internal voltage upward, pushing it toward the threshold where it fires its own impulse.
Inhibitory messengers work the opposite way. GABA, the brain’s main inhibitory messenger, opens channels that let negatively charged chloride ions flow in, pulling the cell’s voltage downward and away from the firing threshold. Your brain constantly balances excitatory and inhibitory signals across billions of synapses to produce coordinated activity. Too much excitation can cause seizures; too much inhibition can dampen consciousness.
Chemical vs. Electrical Synapses
The chemical synapse described above is the most common type, but a second type exists: the electrical synapse. Instead of releasing chemical messengers, electrical synapses connect two cells directly through protein channels called gap junctions. Ions and small molecules pass straight from one cell’s interior to the next, making transmission essentially instantaneous with no delay.
Electrical synapses are also bidirectional. A signal can travel in either direction through the same junction, while chemical synapses are one-way by design. The tradeoff is flexibility. Chemical synapses can amplify, dampen, or modify signals in complex ways. Electrical synapses are faster and more reliable, which is why they often show up in circuits that control escape reflexes, where speed matters more than subtlety. Both types are found throughout the nervous systems of vertebrates and invertebrates.
How Synapses Strengthen and Weaken
Synapses are not fixed connections. Their strength changes depending on how often and how intensely they are used, a property called synaptic plasticity. In the early 1970s, researchers discovered that a few seconds of rapid, repeated stimulation at certain brain synapses could boost signal strength for days or even weeks. This phenomenon, called long-term potentiation, is one of the leading explanations for how the brain stores memories.
Long-term potentiation has several features that make it well suited for learning. It is state-dependent: the receiving cell has to be active at nearly the same moment the sending cell fires, within about 100 milliseconds. This ensures that only signals arriving together get strengthened, a neural version of “neurons that fire together, wire together.” It is also input-specific, meaning only the particular synapse that was active gets stronger, not every connection on the same cell. And it is associative: a weak input that wouldn’t normally trigger strengthening can be boosted if it fires at the same time as a strong neighboring input, allowing the brain to link related pieces of information.
The reverse process also occurs. Synapses that are rarely used gradually weaken, a mechanism called long-term depression. Together, strengthening and weakening allow the brain to continuously reshape its circuits based on experience.
Synaptic Pruning During Development
Babies are born with roughly 100 billion neurons, about 15% more than they will carry into adulthood. Synapse numbers climb rapidly after birth, peaking around age 1 to 2 at about 50% above adult levels. After that early explosion of connectivity, the brain begins trimming back. Synapses that are frequently used get reinforced and retained. Those that are rarely activated weaken and are eventually removed.
Psychiatrist Irwin Feinberg coined the term synaptic “pruning” in 1983, drawing an analogy to trimming a rosebush: cutting away weaker branches lets the remaining ones grow stronger and more stable. This pruning continues aggressively through childhood and adolescence, then stabilizes in adulthood with a possible slight decline in old age. Computational models suggest this pattern, rapid early elimination followed by a slower taper, optimizes the brain’s capacity to carry information. It is one reason why childhood experiences shape brain wiring so powerfully, and why adolescence is a period of significant cognitive and emotional change.
Why Synapses Matter for Health
Because synapses are where brain cells communicate, they sit at the center of many neurological and psychiatric conditions. In Alzheimer’s disease, synapse loss in memory-related brain regions is one of the earliest measurable changes, often appearing before significant cell death. In conditions like epilepsy, the balance between excitatory and inhibitory synapses shifts in ways that allow abnormal bursts of activity. Many psychiatric medications, including antidepressants and anti-anxiety drugs, work by altering how chemical messengers behave at the synapse, either slowing their removal from the cleft or changing how receptors respond to them.
Understanding synapses also helps explain everyday experiences. The fatigue you feel after intense concentration reflects, in part, the depletion of chemical messenger supplies at heavily used synapses. The improvement you see when practicing a skill reflects synaptic strengthening in the relevant circuits. At every level, from molecular machinery to whole-brain function, the synapse is where the action happens.