The synapse is where neurons talk to each other. At these microscopic junctions — typically 20–40 nanometers across — an electrical signal in one neuron is converted into a chemical message, transmitted across the synaptic cleft, and reconverted into an electrical signal in the receiving neuron. With an estimated 100 trillion synapses in the human brain, these connections form the physical substrate of all neural computation, from reflexes to reasoning. The synapse's ability to change its strength in response to activity — synaptic plasticity — is widely believed to be the cellular basis of learning and memory.
Key Structures
- Neurons (throughout nervous system) — The electrically excitable cells that process and transmit information through electrical and chemical signaling.
- Long-Term Potentiation — A persistent strengthening of synapses based on recent patterns of activity — widely considered the cellular mechanism underlying learning and memory.
Key Functions
- Transmits electrochemical signals between neurons via neurotransmitter release.
- the cellular basis of learning and memory.
Chemical Synaptic Transmission
At a chemical synapse, an action potential arriving at the presynaptic terminal triggers the opening of voltage-gated calcium channels. The resulting calcium influx causes synaptic vesicles — small membrane-bound packets containing neurotransmitter molecules — to fuse with the presynaptic membrane and release their contents into the synaptic cleft (exocytosis). Neurotransmitter molecules diffuse across the cleft in less than a millisecond and bind to receptor proteins on the postsynaptic membrane, opening ion channels that produce excitatory or inhibitory postsynaptic potentials. The signal is terminated by enzymatic degradation, reuptake into the presynaptic terminal, or diffusion away from the cleft.
Synaptic Plasticity
Synapses are not fixed connections — their strength can increase (potentiation) or decrease (depression) depending on patterns of activity. Long-term potentiation (LTP) and long-term depression (LTD) are the best-studied forms of synaptic plasticity. LTP, typically induced by high-frequency stimulation, involves increased neurotransmitter release, insertion of additional postsynaptic receptors, and growth of new dendritic spines. Donald Hebb's famous postulate — "neurons that fire together wire together" — anticipated these discoveries by decades and remains a central organizing principle in neuroscience.
Not all synapses are chemical. Electrical synapses (gap junctions) directly connect the cytoplasm of two neurons through protein channels called connexons, allowing ions and small molecules to pass between cells. Electrical synapses transmit signals faster than chemical synapses and can synchronize the activity of neuronal populations. They are particularly important in circuits requiring rapid, coordinated firing, such as the escape reflexes of fish and the synchronized oscillations of inhibitory interneurons that generate brain rhythms.
The Synapse as Drug Target
Because synaptic transmission involves multiple molecular steps, synapses are the primary targets of psychoactive drugs and most psychiatric medications. SSRIs (selective serotonin reuptake inhibitors) treat depression by blocking serotonin reuptake. Benzodiazepines reduce anxiety by enhancing GABA receptor function. Amphetamines increase dopamine release. Understanding synaptic mechanisms has transformed psychiatry and pharmacology, though the complexity of synaptic signaling means that drug effects are often less specific than researchers would like.
Disorders
- Myasthenia gravis (autoimmune synapse attack)
- Alzheimer's disease (synapse loss) — A progressive neurodegenerative disease characterized by memory loss, cognitive decline, and personality changes — the most common cause of dementia in older adults.
- Drug addiction (synapse remodeling)
- Depression — Mood disorder with pervasive sadness and anhedonia; cognitive symptoms include difficulty concentrating, memory problems, and negative cognitive biases.