14.13
Chemical Synapses
Chemical synapses are specialized sites between two neurons or between a neuron and a non-neuronal cell like a muscle, glandular or sensory cell.
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Chemical synapses are specialized sites where electrical signals from a presynaptic neuron are relayed by chemical messengers, known as neurotransmitters, to the postsynaptic cell to propagate an electrical impulse.
They consist of an axon terminal of a presynaptic cell, here a neuron, containing numerous neurotransmitter-filled synaptic vesicles, a postsynaptic cell, in this case, another neuron, with neurotransmitter receptors, and the synaptic cleft, a fluid-filled space between the two.
The unidirectional information transfer at a chemical synapse begins with the arrival of an action potential at the axon terminal of the presynaptic neuron. The resulting membrane depolarization triggers voltage-gated calcium channels to open, allowing calcium ions to rush in. This calcium surge causes the synaptic vesicles to fuse with the presynaptic membrane and release neurotransmitters into the synaptic cleft.
After diffusing through the synaptic cleft, the neurotransmitters bind to specific ion channels on the postsynaptic membrane. This binding opens specific ion channels, allowing appropriate ions to enter the postsynaptic cell and initiate excitatory or inhibitory responses.
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Q1: What are the main structural components of a chemical synapse?
A chemical synapse consists of three key structures: the axon terminal of the presynaptic neuron containing neurotransmitter-filled synaptic vesicles, the postsynaptic cell with neurotransmitter receptors, and the synaptic cleft, a fluid-filled space typically 20-50 nanometers wide separating the two membranes. These components work together to enable chemical communication between neurons.
Q2: How does an action potential trigger neurotransmitter release at a chemical synapse?
When an action potential reaches the presynaptic axon terminal, it depolarizes the membrane and opens voltage-gated calcium channels. Calcium ions rush into the cell, initiating a signaling cascade that causes synaptic vesicles to fuse with the presynaptic membrane, releasing neurotransmitters into the synaptic cleft.
Q3: What happens after neurotransmitters bind to postsynaptic receptors?
When neurotransmitters diffuse across the synaptic cleft and bind to specific receptors on the postsynaptic membrane, they open ligand-gated ion channels. This allows ions to enter the postsynaptic cell, producing excitatory and inhibitory effects of neurotransmitters that either increase or decrease the postsynaptic membrane potential.
Q4: Why is chemical synaptic transmission unidirectional?
Chemical synaptic transmission is unidirectional because neurotransmitters are released only from the presynaptic neuron's axon terminal and receptors are located only on the postsynaptic membrane. This structural arrangement ensures signals travel in one direction, from the presynaptic to the postsynaptic cell.
Q5: What is the synaptic delay and why does it occur?
The synaptic delay is approximately one millisecond between when an action potential reaches the presynaptic terminal and when neurotransmitters open postsynaptic ion channels. This delay occurs because neurotransmitters must be released from vesicles, diffuse across the synaptic cleft, and bind to receptors before the postsynaptic response begins.
Q6: How does the number of released neurotransmitter vesicles affect the postsynaptic response?
Depending on the signal, few or many neurotransmitter vesicles may be released into the synaptic cleft. This variable release regulates neurotransmitter availability, allowing the synapse to fine-tune the neuronal signal and produce either stronger or weaker excitatory or inhibitory postsynaptic responses.
Q7: How do autoimmune disorders disrupt normal chemical synaptic function?
In Lambert-Eaton myasthenic syndrome, antibodies target voltage-gated calcium channels, reducing neurotransmitter release and causing muscle weakness. In myasthenia gravis, autoantibodies block acetylcholine from binding postsynaptic receptors at the neuromuscular junction, preventing muscle contraction and causing facial weakness and diminished expression.