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Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
Because chemical synapses depend on the release of neurotransmitter molecules from synaptic vesicles to pass on their signal, there is an approximately one millisecond delay between when the axon potential reaches the presynaptic terminal and when the neurotransmitter leads to opening of postsynaptic ion channels. Additionally, this signaling is unidirectional.
A synaptic cleft, usually 20-50 nm wide, separates the pre-and postsynaptic membranes. When an action potential reaches the axon terminal, it depolarizes the membrane and opens voltage-gated sodium channels. Sodium ions enter the cell, further depolarizing the presynaptic membrane. This depolarization causes voltage-gated calcium channels to open. Calcium ions entering the cell initiate a signaling cascade that causes small membrane-bound vesicles, called synaptic vesicles, containing neurotransmitter molecules to fuse with the presynaptic membrane.
Fusion of a vesicle with the presynaptic membrane causes neurotransmitter to be released into the synaptic cleft, the extracellular space between the presynaptic and postsynaptic membranes. The neurotransmitter diffuses across the synaptic cleft and binds to receptor proteins on the postsynaptic membrane. The binding of a specific neurotransmitter causes particular ion channels, like ligand-gated channels, on the postsynaptic membrane to open. Neurotransmitters can either have excitatory or inhibitory effects on the postsynaptic membrane.
Once neurotransmission has occurred, the neurotransmitter must be removed from the synaptic cleft so the postsynaptic membrane can "reset" and be ready to receive another signal.
Depending on the signal, a few or many neurotransmitter vesicles may be released, bringing about an excitatory or inhibitory postsynaptic response. This can result in an increased or decreased postsynaptic membrane potential depending on the bound neurotransmitter. Additionally, as the neurotransmitters' availability in the synaptic cleft is regulated, this helps fine-tune the neuronal signal.
Clinical Relevance
Lambert-Eaton myasthenic syndrome is an autoimmune disorder wherein antibodies are targeted against the voltage-gated calcium channels that trigger the acetylcholine neurotransmitter release. Thus, the lowered levels of acetylcholine are insufficient to cause regular muscle contractions, resulting in muscle weakness.
In Myasthenia gravis, another autoimmune syndrome, in which autoantibodies block the acetylcholine from binding the postsynaptic membrane receptor at the neuromuscular junction, inhibiting contraction. This predominantly results in muscle weakness and diminished facial expression.
This text is adapted from Openstax, Biology 2e, Section 35.2 How Neurons Communicate.
