What occurs when there is a lack of acetylcholinesterase in the synaptic vesicles?

The presence and functioning of acetylcholinesterase at the neuromuscular junction are crucial for muscle contraction and relaxation. Acetylcholinesterase is an enzyme responsible for breaking down acetylcholine, a neurotransmitter that stimulates muscle contractions.

When there is a lack of acetylcholinesterase, acetylcholine remains in the synaptic cleft for a longer duration than normal because it is not being degraded effectively. This leads to continuous stimulation of the muscle fibers, resulting in persistent contraction. Therefore, muscles become overactivated and are unable to relax properly, ultimately causing spastic paralysis. In this state, individuals may experience muscle stiffness and cramps, as the muscles are stuck in a contracted state.

This scenario contrasts with other outcomes such as muscle atrophy, which results from disuse or denervation rather than a lack of acetylcholinesterase, or flaccid paralysis, which occurs when there is insufficient stimulation of the muscles. Therefore, the lack of acetylcholinesterase clearly leads to spastic paralysis due to the inability to terminate the action of acetylcholine effectively.