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Calcium triggers synaptic vesicles to discharge the neurotransmitter into the synaptic cleft.
They don't, the neurotransmitters stay on either side of the synapse. Neurotransmitters are released when the synaptic vesicles fuse with the presynaptic neuron's membrane, so as to release them into the synaptic cleft.
When presynaptic cells produce action potentials, it triggers the opening of voltage-gated calcium channels in the presynaptic membrane. This influx of calcium ions into the presynaptic cell triggers the release of neurotransmitter molecules from small, membrane-bound vesicles. The released neurotransmitters then diffuse across the synapse and bind to receptors on the postsynaptic cell, generating a response in the postsynaptic cell.
Yes, Autoreceptors are located at the receptor site on the presynaptic neuron. They provide feedback on the amount of neurotransmitter release in the synaptic cleft in order to regulate its level through the activity of G proteins and second messengers.
Calcium ions cause the neurotransmitter vesicles to fuse with the axon terminal. When an action potential reaches the axon terminal, voltage-gated calcium ion pores are opened, allowing calcium ions into the axon terminal. These ions initiate the release of neurotransmitter vesicles stored on elements of the cytoskeleton located near the presynaptic membrane; they then travel to the presynaptic membrane, where they first dock, and then fuse with the presynaptic membrane, forming an opening or pore through which the neurotransmitters are released into the synaptic cleft.
An action potential travels down the neuron and reaches the presynaptic knob. This causes the Calcium ion channels to open and allow an influx of calcium into the knob. The increased concentration of calcium causes the secretory vesicles within the knob to bind to the outer membrane and release their neurotransmitter (e.g. ACh) into the synaptic cleft.
Sodium ions
Presynaptic neurons release the neurotransmitter in response to an action potential. Postsynaptic neurons receive the neurotransmitter (and can however become presynaptic to the next nerve cell, if the neurotransmitter has stimulated the cell enough).
an action will happen cause of axo-axonal syanapse,which can facilitate the nerve impulse transmitting from presynaptic membrane to post synaptic membrane. In the axo-axonal synapse one axon is secreting serotonin which can influence to close some of K+ channels in the other neuron to maintain a prolonged action potential by slowing down the repolarization. as long as action potential is there it can stimulate the presynaptic membrane to release neurotransmitters towards postsyanptic membrane so prolonged action potential will help to stimulate more the Post synaptic membrane and give a strong impulse this is called presynaptic facilitation
When the action potential reaches the button(axon terminal) of the presynaptic neuron the depolarization causes voltage gated calcium channels to open increasing intracellular calcium content. This causes synaptic vesicles to fuse to the membrane and release neurotransmitters that bind to the post synaptic neuron and create a chemical action potential.
After the action potential reaches the presynaptic terminal, voltage-gated calcium channels open, leading to an influx of calcium ions. This triggers the release of neurotransmitters into the synaptic cleft. These neurotransmitters then bind to receptors on the postsynaptic membrane, leading to depolarization and the generation of a new action potential in the postsynaptic neuron.
One example is the membrane phospholipid PIP2. When the receptor is activated, the PIP2 will by hydrolyzed by phospholipase C into DAG and Inositol triphosphate (IP3).DAG is insoluble so it stays in the membrane. It stimulates the production of protein kinase C which phosphorylates a protein to generate a second messenger.iP3 is soluble so it binds to the receptors. This triggers the release of mitochondrial calcium and it hence triggers a cellular response.