Leaves the presynaptic neuron, activates ion channel
The sites where a chemical substance is transmitted from the presynaptic terminal of an axon to the postsynaptic membrane of a muscle fiber are called neuromuscular junctions. At these junctions, the neurotransmitter acetylcholine is released from the presynaptic terminal and binds to receptors on the postsynaptic membrane, initiating muscle contraction.
The calcium ion is responsible for causing the presynaptic vesicle to fuse to the axon membrane in a process called exocytosis. When an action potential reaches the presynaptic terminal, calcium ions enter the terminal and trigger the fusion of the vesicle with the axon membrane, releasing neurotransmitters into the synaptic cleft.
When an action potential arrives at the presynaptic terminal, voltage-gated calcium channels open, allowing calcium ions to enter the cell. The influx of calcium triggers the release of neurotransmitter vesicles from the presynaptic terminal into the synaptic cleft. These neurotransmitters then bind to receptors on the postsynaptic membrane, leading to changes in the postsynaptic cell's membrane potential.
The axon terminals of a neuron form the presynaptic neuronal membrane. These structures contain synaptic vesicles that store neurotransmitters for release at the synapse.
The synapse consists of two main parts that allow one neuron to communicate with another: 1) the presynaptic terminal located at the end of an axon; and 2) the postsynaptic terminal located on the dendrite of another neuron. The presynaptic terminal is where neurotransmitters are stored and released from. The postsynaptic terminal is the recipient side of the synapse. Neurotransmitters released from the presynaptic terminal will diffuse across the synaptic cleft and bind to receptors located on the surface of dendritic spines.
Calcium ions (Ca²⁺) must flow into the presynaptic cell for neurotransmitter release. When an action potential reaches the presynaptic terminal, voltage-gated calcium channels open, allowing Ca²⁺ to enter the cell. This influx of calcium triggers the fusion of neurotransmitter-containing vesicles with the presynaptic membrane, leading to the release of neurotransmitters into the synaptic cleft.
Botulinus toxin blocks the release of acetylcholine from the presynaptic terminal. This is a total blockage of neuronal transmission.
An autoreceptor is a receptor which is situated in the terminal of a presynaptic nerve cell, sensitive to neurotransmitters released by the neuron in whose membrane the autoreceptor sits.
Neurotransmitters are typically synthesized and stored in the synaptic vesicles of the presynaptic terminal, which is located at the end of the neuron. When an action potential arrives, these vesicles release neurotransmitters into the synaptic cleft to communicate with the postsynaptic neuron.
Let's picture a presynaptic neuron, a synaptic cleft, and a postsynaptic neuron. An action potential reaches the terminal of a presynaptic neurone and triggers an opening of Ca ions enters into the depolarized terminal. This influx of Ca ions causes the presynaptic vesicles to fuse with the presynaptic membrane. This releases the neurotransmitters into the synaptic cleft. The neurotransmitters diffuse through the synaptic cleft and bind to specific postsynaptic membrane receptors. This binding changes the receptors into a ion channel that allows cations like Na to enter into the postsynaptic neuron. As Na enters the postsynaptic membrane, it begins to depolarize and an action potential is generated.
Presynaptic inhibition is the opposite of presynaptic facilitation. In presynaptic inhibition, the release of neurotransmitters from the presynaptic neuron is reduced, leading to a decrease in synaptic transmission. In contrast, presynaptic facilitation enhances neurotransmitter release, increasing the strength of synaptic transmission.