Neurotransmitters are released from the nerve terminals by a specialized exocytosis process, synaptic vesicles. These are small nearly uniform capsules that join with the cell membrane to expel their contents. Release is both quantal (set amount) and mediated by calcium.
exocytosis
Calcium triggers synaptic vesicles to discharge the neurotransmitter into the synaptic cleft.
Neurotransmitters are stored in synaptic vesicles within axonal terminals for release into the synaptic cleft.
"When a nerve impulse reaches the synaptic knob at the end of an axon, synaptic vesicles release a neurotransmitter that diffuses across the synaptic cleft and binds to specific receptors on the postsyanptic membrane" Above From:Hole's essentials of Human Anatomy & Physiology (tenth edition) page=220, figure9.9 Quick definition of the "Synaptic knob- Tiny enlargement at the end of an axon that secretes a neurotransmitter." Above From: Same book as before (Hole's essentials of Human...) page= 584 (Glossary)
Synaptic vesicles store neurotransmitters to be released into the synapses. In the case of most motoneurons, this neurotransmitter is acetylcholine (ACh). The neurons that interface with the sympathetic nervous system, also technically motoneurons, release norepinephrine.
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.
Calcium triggers synaptic vesicles to discharge the neurotransmitter into the synaptic cleft.
Calcium ions enter the presynaptic neuron resulting in the release of neurotransmitter from the per-synaptic membrane. The neurotransmitter diffuses across the synaptic cleft, fusing with the receptors of the post-synaptic membrane. This changes the sodium channels to open and sodium ions will to flow into the post-synaptic neuron, depolarizing the post-synaptic membrane. This initiates an action potential. After the post-synaptic neuron has been affected, the neurotransmitter is removed by a type of enzyme called cholinesterase. The inactivated neurotransmitter then returns to the pre-synaptic neuron.
The cause of synaptic delay is attributed mainly to the time needed for the synaptic vesicles to release neurotransmitter into the synaptic cleft. While it can be considered a combination of binding to the presynaptic membrane (which is relatively a transient process) and subsequent exocytosis of the neurotransmitter, the main factor is release. Additionally, it does take a very short period of time for the neurotransmitter to diffuse across the synaptic cleft and bind to to its receptors on the post-synaptic membrane.
Most neurons have a chemical synapse, which is to say that a substance called a neurotransmitter is released from the first neuron (called pre-synaptic) to the next neuron called (post-synaptic). How is the release triggered? When an action potential reaches the terminus (end of the axon) there are specialized calcium channels that are opened (voltage-gated). The calcium bind so the inner membrane and triggers the release of small membrane bound vesicles which spill out their contents of neurotransmitter into the synaptic cleft. The neurotransmitter binds to specific receptors on the post-synaptic membrane and that causes the action potential to propagate on (or for the neurotransmitter to cause an action like a muscle contraction).
Reuptake, or re-uptake, is the reabsorption of a neurotransmitter by a neurotransmitter transporter of a pre-synaptic neuron after it has performed its function of transmitting a neural impulse.Reuptake is necessary for normal synaptic physiology because it allows for the recycling of neurotransmitters and regulates the level of neurotransmitter present in the synapse and controls how long a signal resulting from neurotransmitter release lasts. Because neurotransmitters are too large and hydrophilic to diffuse through the membrane, specific transport proteins are necessary for the reabsorption of neurotransmitters. Much research, both biochemical and structural, has been performed to obtain clues about the mechanism of reuptake.
Reuptake, or re-uptake, is the reabsorption of a neurotransmitter by a neurotransmitter transporter of a pre-synaptic neuron after it has performed its function of transmitting a neural impulse.Reuptake is necessary for normal synaptic physiology because it allows for the recycling of neurotransmitters and regulates the level of neurotransmitter present in the synapse and controls how long a signal resulting from neurotransmitter release lasts. Because neurotransmitters are too large and hydrophilic to diffuse through the membrane, specific transport proteins are necessary for the reabsorption of neurotransmitters. Much research, both biochemical and structural, has been performed to obtain clues about the mechanism of reuptake.
Ca2+
By a chemical released by an axon.
Neurotransmitters are stored in synaptic vesicles within axonal terminals for release into the synaptic cleft.
"When a nerve impulse reaches the synaptic knob at the end of an axon, synaptic vesicles release a neurotransmitter that diffuses across the synaptic cleft and binds to specific receptors on the postsyanptic membrane" Above From:Hole's essentials of Human Anatomy & Physiology (tenth edition) page=220, figure9.9 Quick definition of the "Synaptic knob- Tiny enlargement at the end of an axon that secretes a neurotransmitter." Above From: Same book as before (Hole's essentials of Human...) page= 584 (Glossary)
There is no neurotransmitter release from the axon terminal when there are no calcium ions in the extracellular solution. This is because the exocytosis of the synaptic vesicles is calcium dependent.
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.