A lack of acetylcholinesterase in the synaptic cleft results in excessive, continuous stimulation of the muscle fiber due to the prolonged presence of acetylcholine. Therefore, the correct option is a. Excessive, continuous stimulation of the muscle fibre .
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Acetylcholinesterase (AChE) is the enzyme responsible for breaking down acetylcholine (ACh) in the synaptic cleft; after ACh is released by motor neurons & binds to receptors on muscle fiber to trigger contraction, AChE terminates the signal by breaking down ACh.
If AChE is deficient, ACh would accumulate in the synaptic cleft & continue to stimulate ACh receptors on the muscle fiber, leading to prolonged depolarization & continuous contraction / spasms.
Lack of acetylcholinesterase can be linked to a few conditions such as:
Organophosphate Poisoning: exposure to pesticides / nerve agents
Myasthenia Gravis (MG): autoimmune destruction of nicotine ACh receptors at neuromuscular junction
Alzheimer’s Disease: deficit in central cholinergic transmission
Succinylcholine O/D: succinylcholine is a depolarizing neuromuscular blocker that mimics ACh, but not broken down by AChE - excess stimulation can cause prolonged depolarization / paralysis, especially in pts w/ pseudocholinesterase deficiency
Cholinergic Crisis: O/D of AChE inhibitors, organophosphate poisoning
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