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Many nerve gasses (e.g., sarin (GB), soman (GD)) were designed to impact acetylcholinesterase. Specifically, what do...

Many nerve gasses (e.g., sarin (GB), soman (GD)) were designed to impact acetylcholinesterase. Specifically, what do these nerve gasses do to this enzyme? How does the change in acetylcholinesterase (brought about by nerve gasses) affect nerve transmission?

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Acetylcholine is a neurotransmitter at the neuromuscular junction. The motor neurons release it to activate muscles, at the autonomic nervous system, and as internal transmitter for the sympathetic nervous system. It is acted upon by the enzyme acetylcholine esterase which breaks it down to acetic acid and choline.

Acetyl choline can bind either to nicotinic or musacarnic receptors. When stimulated, a motor nerve releases acetylcholine. Once the impulse is transmitted, the enzyme acetylcholineesterase degrades it to allow the muscles to relax.

Sarin acts as a modulator of the enzyme, they allow enzyme substrate complex to form but inhibit the release of the product. As a result, persistent present of acetylcholine makes the nerve impulse continuously transmitted. Muscle contractions do not stop, and they remain in spasmic state.

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