Vesicles containing the neurotransmitters are caused to fuse with the neuron's cell membrane, which thereby presents the neurotransmitters to the outside of the neuron, into the synapse.
As I'm sure you know a neurotransmitter is how two neurons communicate at a synapse. It can be one of many molecules, often nor-epinephrine/nor-adrenaline. Neurotransmitters are stored in structures called vesicles in a bulb at the end of the axon the presynaptic neuron. These vesicles are like balloons containing the neurotransmitters, what would be the rubber of the balloon is actually made of the same plasma membrane that surrounds the rest of the cell. When the Action Potential (AP) coming down the axon gets to the bulb it causes Ca ion channels to open. These channels are membrane bound proteins ant act as voltage gated channels in the same way the Sodium ion channels in the axon do. The opening of these channels allows calcium entry into the cells. There are another class of membrane bound proteins that are important here, the Docking proteins. Ca ions activate the docking proteins by binding to them. What these proteins do is effectively grab the vesicles, containing the neurotransmitter, and make the membrane merge with the cells membrane. This is exactly like the opposite of phagocytosis, the cell then secretes the neurotransmitter into the synaptic cleft.
The neurotransmitter must then & isreleased from the receptor site, in order to prevent continuing and constant over-stimulation of the post-synaptic neuron. It can be carried back to the presynaptic neuron for either repackaging into vesicles or broken down there by enzymes, or some neuropeptide neurotransmitters simply diffuse away into the surrounding medium, and one (acetylcholine) is broken down right in the synaptic cleft.
Electrical stimulation of the nerve cell, down the dendrite and to the synapse, once released it has to find a sympathetic receptor cite across the synapse for it to transmit, and so on and so on to elaborate the single cell activation into the multiple activation which then allows function.
Brain, thinking, muscle activation-whatever, or wherever the cells are
Norepinephine- which is released at synaptic nerve endings, responds to hypotension and physical stress.
Acetylcholine is released at SOME synapses in the spinal cord and at neuromuscular junctions; it influences muscle action.
When a threshold stimulus is presented to the neuron, it is depolarized, making it possible for the neurotransmitter to be released into the synaptic cleft.
acecylocholine
Calcium channel gate open
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.
acetylcholine
Neurotransmitter diffuses across the synaptic cleft to bind to the receptor on the muscle or next nerve.It is then broken down and absorbed back into the nerve.NovaNET answer: quickly destroyed..........Good Luck :)
Neurotransmitters are stored in synaptic vesicles in the terminal bouton of pre-synaptic axons. They are released from the terminal bouton into the synaptic cleft and the neurotransmitters exert their action on the post-synaptic neurons.
Ca2+
Calcium triggers synaptic vesicles to discharge the neurotransmitter into the synaptic cleft.
simple diffusion
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.
In general, action potentials that reach the synaptic knobs cause a neurotransmitter to be released into the synaptic cleft. The arrival of the action potential opens voltage-sensitive calcium channels in the presynaptic membrane.
prevent transmission across the synaptic cleft
Neurotransmitters are stored in synaptic vesicles within axonal terminals for release into the synaptic cleft.
acetylcholine
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 synaptic knob contains vesicles filled with neurotransmitters. Therefore, Acetylcholine is the neurotransmitter that stimulates skeletal muscle to contract. It is released into the synaptic clefts between motor neuron axons and motor end plates.
Calcium (Ca2+) channels open on the synaptic end bulb in response to depolarization (from the action potential), inducing exocytosis of synaptosomes containing neurotransmitter, resulting in neurotransmitter being released into the synaptic cleft...further propagating the signal to the next neuron or set of neurons.
An electrial nerve impulse travels across a synapse by diffusion. The neurotransmitter substance from the pre-synaptic cleft travels across the synapse via diffusion. This is then received by receptors in the post synaptic cleft