Acetylcholinesterase (AChE) is a cholinergic enzyme primarily found at postsynaptic neuromuscular junctions, especially in muscles and nerves. It immediately breaks down or hydrolyzes acetylcholine (ACh), a naturally occurring neurotransmitter, into acetic acid and choline.
Besides, what would happen if acetylcholinesterase were blocked?
The inhibition of the enzyme leads to accumulation of ACh in the synaptic cleft resulting in over-stimulation of nicotinic and muscarinic ACh receptors and impeded neurotransmission. The typical symptoms of acute poisoning are agitation, muscle weakness, muscle fasciculations, miosis, hypersalivation, sweating.
Secondly, is neostigmine reversible or irreversible?
The chemical structure of classic, reversible inhibitors physostigmine and neostigmine shows their similarity to acetylcholine. Edrophonium is also a reversible inhibitor. These compounds have a high affinity with the enzyme, and their inhibitory action is reversible.
What triggers acetylcholinesterase?
When a motor nerve cell gets the proper signal from the nervous system, it releases acetylcholine into its synapses with muscle cells. There, acetylcholine opens receptors on the muscle cells, triggering the process of contraction.
Acetylcholinesterase catalyzes the breakdown of acetylcholine molecules once the communication between cells is complete. This is an essential function. Compounds like Sarin and VX nerve agents, which inhibit the action of acetylcholinesterase, are highly toxic, and fatal even in small quantities.
Excessive accumulation of acetylcholine (ACh) at the neuromuscular junctions and synapses causes symptoms of both muscarinic and nicotinic toxicity. These include cramps, increased salivation, lacrimation, muscular weakness, paralysis, muscular fasciculation, diarrhea, and blurry vision.
After the release of acetylcholine from vesicles, it binds to post-synaptic receptors and is then broken down by the enzyme acetylcholinesterase. However, when anticholinesterases bind to the enzyme, they prevent the neurotransmitter from being broken down. Acetylcholine continues to activate its receptor.
Severe cholinesterase inhibition can result in death primarily because of respiratory failure. This failure results from a combination of bronchial secretions, bronchial constriction, weakened respiratory muscle function, and inhibited respiratory drive.
In fish, brain and muscle tissue contain mostly AChEs, while liver and plasma contain mostly BChEs . Significant amounts of BChE activity, however, have been reported in the muscle tissues of several fish species [8, 9].
Some drugs known to be associated with drug-induced drooling or sialorrhea. Indirect muscarinic stimulants are primarily inhibitors of the acetylcholinesterase enzyme, they increase acetylcholine to stimulate muscarinic and nicotinic receptors which results in an increased saliva flow.
Acetylcholine itself does not have therapeutic value as a drug for intravenous administration because of its multi-faceted action (non-selective) and rapid inactivation by cholinesterase.