My guess is that it gets hydrolyzed to choline and acetic acid
Acetylcholine (ACh) is released from the presynaptic neuron into the synaptic cleft. It then binds to ACh receptors on the postsynaptic neuron, causing ion channels to open and allowing for the transmission of the nerve impulse. Any remaining ACh is broken down by the enzyme acetylcholinesterase, ensuring that the signal is quickly terminated.
Acetylcholine is degraded by acetylcholinesterase
Acetylcholine (ACh) does not remain on the post-synaptic membrane because it is rapidly broken down by the enzyme acetylcholinesterase. This enzymatic degradation occurs in the synaptic cleft, preventing prolonged stimulation of the post-synaptic receptors. Additionally, the reuptake of choline into the pre-synaptic neuron helps recycle components for future neurotransmitter synthesis. This process ensures that synaptic transmission is brief and precisely regulated.
Acetylcholinesterase (AChE) is an enzyme that breaks down acetylcholine (ACh) into choline and acetate, thus destroying ACh. This process helps in regulating the levels of ACh at the synaptic cleft and terminating its action.
Acetylcholine (ACh) is removed from the synaptic cleft through a process called enzymatic degradation. The enzyme acetylcholinesterase breaks down ACh into its components, acetate and choline, which are then taken back up into the presynaptic neuron for recycling or further processing.
it blocks things [such as acetylchoinesterase] that break down ach
At a neuromuscular junction, the process begins when an action potential travels down a motor neuron, leading to the release of acetylcholine (ACh) from synaptic vesicles into the synaptic cleft. ACh binds to receptors on the muscle cell membrane, causing depolarization and the initiation of an action potential in the muscle fiber. This depolarization triggers the release of calcium ions from the sarcoplasmic reticulum, ultimately leading to muscle contraction. The ACh is then broken down by the enzyme acetylcholinesterase, terminating the signal and allowing the muscle to relax.
acetylcholinesterase destroying the ACh
Acetylcholinesterase destroying the ACH
Neostigmine is a competitive irreversible inhibitor of Acetylcholinesterase (AChE), an enzyme responsible for breaking down acetylcholine (ACh). Myasthenia gravis is caused by the body producing too little ACh receptors. As stimulating the ACh receptors is needed for nervous transmission, the nerve signals cannot be transmitted causing muscle weakness and fatigue. Neostigmine is hence used to inhibit AChE so that less ACh gets broken down. This leads to more ACh binding to the ACh receptors causing muscular contraction.
Physostigmine inhibit AchE (the enzyme that hadrolyse Ach), so Ach accumulate at synaptic cleft and banish the effect of atropine
In a neuromuscular junction, synaptic vesicles in the motor neuron contain the neurotransmitter acetylcholine (ACh). When an action potential reaches the motor neuron, ACh is released into the synaptic cleft and binds to receptors on the muscle fiber, leading to muscle contraction.