choline esterase enzyme and there is 2 types of choline esterase 1 .truecholine esterase 2. pseudo choline esterase
acetylcholinesterase
acetylcholine esterase
Acetylcholinesterase
most neurotransmitters are not actually broken down, rather they are actively transported back into their pre release vesicles (this is called reuptake). Some neurotransmitters are broken down by a specific enzyme into non active parts i.e acetylcholine broken down by acetylcholinestarase
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 :)
Synapse: neurotransmitters from the pre-synaptic membrane spill into the synaptic cleft (synaptic gap), where the electrical impulse is transferred to the dendrites of the post-synaptic membrane.
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.
Afferent neurons go to the Brain while efferent neurons go down
Acetylcholine is degraded by acetylcholinesterase
Acetylcholine is a neurotransmitter that does not go through the reuptake process. Instead, it is broken down by an enzyme called acetylcholinesterase in the synaptic cleft.
Acetycholine is broken down into acetate and choline in the synaptic cleft.
most neurotransmitters are not actually broken down, rather they are actively transported back into their pre release vesicles (this is called reuptake). Some neurotransmitters are broken down by a specific enzyme into non active parts i.e acetylcholine broken down by acetylcholinestarase
Also known as AChE, Acetylcholinesterase is an enzyme that breaks down the neurotransmitter acetylcholine, resulting in choline and an acetate group. This occurs at the synaptic cleft. Too much acetylcholine can lead to paralysis
Physostigmine is an inhibitor of acetylcholinesterase which breaks down acetylcholine in the synaptic cleft of the neuromuscular junction. It is used in the treatment of Alzheimer's and memory loss.
To provide energy for the re-combination of Choline and ethanoic acid, to form Acetylcholine. Acetylcholine is used as a neurotransmitter, and gets broken down after its reached the sodium channels' receptors on the post-synaptic membrane by acetylcholinease.
Most neurotransmitters are removed by being taken up by the presynaptic or postsynaptic neurones however acetylcholine is the prime exeption to this as is actually destroyed in the synaptic cleft by the enzyme acetylcholinesterase. The reason this must happen is that otherwise the neurotransmitter would be left in the cleft where it would continue to evoke a response in the postsynaptic cell for longer than it should. For this reason reuptake and catabolic enzymes are often the targets of drugs gieven to treat neurological disorders. Another possible problem is wastage, if the neurotransmitter is left in the cleft it may difuse away and be wasted giving the presynaptic neurone more work to do creating more.
The NMJ is the region where the efferent motor nerves connect with muscle tissue. When a signal is sent from the brain, down the spinal cord, to the nerve, neurotransmitters are released into the synaptic cleft (primary acetylcholine), which cause the muscle to contract.
Nerve impulses are transmitted down the axon and leave the neuron via the terminal bouton at the synaptic interface, releasing neurotransmitters into the synaptic cleft to affect the post-synaptic cell..
This is the neuromuscular junction. The action potential travels down the presynaptic motor neuron, releasing acetylcholine (ACh), which cross the synapse (neuromuscular junction), to bind to receptors on the end plate of muscle fibers, which induces depolarization, causing the muscle to contract.
The process is called re-uptake , in the synaptic cleft certain medicines interfere with the process where excess neurotransmitters are left in the synaptic cleft , they are reabsorbed and they are broken down by enzymes. If this process is interfered with, the neurotransmitters are left to reexcite the receptors on the dendrites of the neurons. (for example) look at prozac, a person has a defeciency of dopeamine the drug interferes with re-uptake thereby making dopeamine more efficient, (Allen Delaine)