What Is a Neuronal Synapse and How Does It Work?
Understand the mechanism of communication between neurons. This process underlies how we learn and remember, and is central to overall neurological function.
The human brain contains approximately 86 billion neurons that communicate through electrical and chemical signals. These points of communication are called synapses, microscopic gaps where a signal passes from a sending neuron to a receiving one. Each neuron can form thousands of these connections with neighboring cells. This transfer of information across trillions of synaptic connections forms the physical basis for all thoughts, memories, emotions, and actions.
Anatomy of a Synapse
A synapse is composed of three parts. The first is the presynaptic terminal, the end of the sending neuron’s axon. This terminal holds neurotransmitters, the nervous system’s chemical messengers, within small spheres called synaptic vesicles. The presynaptic terminal also contains a high concentration of mitochondria to supply the energy needed for communication.
Facing the presynaptic terminal is the postsynaptic terminal, located on a dendrite or the cell body of the receiving neuron. Its membrane is equipped with a dense collection of proteins called receptors. Each receptor is shaped to recognize and bind with a specific neurotransmitter, similar to how a key fits into a lock, allowing the cell to interpret the message.
Between the presynaptic and postsynaptic terminals is a narrow gap known as the synaptic cleft. This space, less than 50 nanometers wide, is filled with fluid and proteins that help hold the two neurons in close proximity. The signal must traverse this cleft, which ensures that communication is precise and that signals travel in one direction.
Synaptic Transmission
Transmitting a signal begins when an electrical impulse, or action potential, reaches the presynaptic terminal. This arrival triggers the opening of channels that allow calcium ions to rush into the cell. The influx of calcium prompts synaptic vesicles filled with neurotransmitters to move toward the edge of the presynaptic terminal.
The vesicles fuse with the membrane and release their contents into the synaptic cleft through exocytosis. These neurotransmitter molecules travel across the gap in microseconds and bind to their corresponding receptors on the postsynaptic terminal. This binding event converts the chemical signal back into an electrical one.
The interaction between neurotransmitters and receptors causes ion channels on the postsynaptic membrane to open, allowing charged particles to flow into or out of the receiving neuron. If the flow of ions makes the inside of the cell more positive, it creates an excitatory postsynaptic potential (EPSP), making the neuron more likely to fire its own action potential. Conversely, if the ion flow makes the cell more negative, it results in an inhibitory postsynaptic potential (IPSP), making it less likely to fire.
A single neuron constantly integrates these incoming excitatory and inhibitory signals from thousands of synapses to determine its overall response. While most synapses are chemical, a small number are electrical. Electrical synapses use channels called gap junctions to allow ions to flow directly between cells, enabling nearly instantaneous and synchronized activity among groups of neurons.
Synaptic Plasticity
Synapses are not fixed structures; they can change their strength over time in response to neural activity. This dynamic process, known as synaptic plasticity, is the mechanism that underlies learning and memory. The brain’s capacity to adapt is tied to the strengthening or weakening of these connections between neurons.
Two primary forms of this plasticity are Long-Term Potentiation (LTP) and Long-Term Depression (LTD). LTP is a persistent strengthening of a synaptic connection that occurs when it is frequently used, making communication more efficient. This process often involves increasing the number of neurotransmitter receptors on the postsynaptic membrane, making it more sensitive to signals.
Conversely, LTD is the long-lasting weakening of a synaptic connection that results from a lack of stimulation or specific patterns of low-frequency activity. During LTD, the number of receptors on the postsynaptic neuron may decrease, making the synapse less responsive. This process is just as important as LTP, as it allows for the pruning of unused or inefficient connections, refining neural circuits.
Synapses in Health and Disease
Proper synaptic function is necessary for neurological health, and disruptions in this activity are linked to many brain disorders. In several neurodegenerative diseases, the loss of synapses is a primary event that occurs before neurons die and is correlated with cognitive symptoms. This synaptic failure can be driven by toxic proteins that interfere with communication.
In Alzheimer’s disease, for example, amyloid-β and tau protein aggregates damage synapses. These oligomers disrupt the release of neurotransmitters and the function of postsynaptic receptors, leading to synapse loss and memory impairment. Parkinson’s disease involves the loss of dopamine-producing neurons and their synapses in brain regions that control movement.
Synapses are a primary target for therapeutic interventions. Many medications for psychiatric disorders, such as depression and anxiety, work by modulating synaptic transmission. Selective serotonin reuptake inhibitors (SSRIs), for instance, increase the amount of the neurotransmitter serotonin in the synaptic cleft by blocking its reabsorption into the presynaptic neuron. This action helps to correct imbalances in serotonergic signaling that are thought to contribute to the symptoms of depression.