What is the action of acetylcholinesterase?

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.

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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.

Keeping this in view, what is the difference between acetylcholine and acetylcholinesterase? The two types of cholinesterase are acetylcholinesterase (ACHE) and butyrylcholinesterase (BCHE). The difference between the two types has to do with their respective preferences for substrates: the former hydrolyses acetylcholine more quickly; the latter hydrolyses butyrylcholine more quickly.

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.

Why is acetylcholinesterase important?

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.

What happens if there is too much acetylcholine?

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.

What happens after acetylcholine is broken down?

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.

Why inhibiting acetylcholinesterase can result in death?

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.

Are there any other organs in fish that may contain acetylcholinesterase?

In fish, brain and muscle tissue contain mostly AChEs, while liver and plasma contain mostly BChEs [6]. Significant amounts of BChE activity, however, have been reported in the muscle tissues of several fish species [8, 9].

Why do acetylcholinesterase inhibitors cause excessive salivation?

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.

Why acetylcholine is not used clinically?

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.

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