My guess is that it gets hydrolyzed to choline and acetic acid
Acetylcholine is degraded by acetylcholinesterase
Synaptic Vesicles
it blocks things [such as acetylchoinesterase] that break down ach
acetylcholinesterase destroying the ACh
The transport process by which ACh is released into the synaptic cleft is called Exocytosis.
Acetylcholinesterase destroying the ACH
Physostigmine inhibit AchE (the enzyme that hadrolyse Ach), so Ach accumulate at synaptic cleft and banish the effect of atropine
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.
Exocytosis. As a result of the influx of Calcium ions, the synaptic vesicles transport the neurotransmitter Ach (Acetylcholine) to the presynaptic membrane, the vesicles fuse to the membrane, and the neurotransmiffer, Ach, diffuses. Once the neurotransmitters cross the synaptic cleft, they bind to the receptors on the post synaptic membrane. Hope it helps a bit.
Synaptic vesicles in the neuromuscular junction contain acetylcholine (ACh) which is the neurotransmitter for initiating muscular contractions.
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.
ACh is produced at the intercellular level and is stored in vesicles at nerve endings. nerve endings release ACh ACh attavhes to the receptor site at the receiving nerve ACh is broken down by AChE to prevent accumulation