Inhibition of acetylcholinesterase by poisoning blocks neurotransmission at the neuromuscular junction because
a. ACh is no longer released by the presynaptic terminal.
b. ACh synthesis in the presynaptic terminal is blocked.
c. ACh is not degraded, so prolonged depolarization is enforced on the postsynaptic cell.
d. ACh is blocked from attaching to the postsynaptic ACh receptors.

Verified step by step guidance

1. Step 1: Understand the role of acetylcholinesterase (AChE) at the neuromuscular junction. AChE is an enzyme responsible for breaking down acetylcholine (ACh) in the synaptic cleft after it has transmitted the signal to the muscle cell.
2. Step 2: Recognize what happens when acetylcholinesterase is inhibited. If AChE is blocked, acetylcholine is not degraded and remains in the synaptic cleft for a longer time.
3. Step 3: Consider the effect of prolonged presence of acetylcholine on the postsynaptic membrane. Continuous presence of ACh causes prolonged activation of ACh receptors, leading to sustained depolarization of the muscle cell membrane.
4. Step 4: Analyze why this prolonged depolarization blocks neurotransmission. Normally, after a brief depolarization, the muscle cell repolarizes to be ready for the next signal. Prolonged depolarization prevents this reset, effectively blocking further neurotransmission.
5. Step 5: Match this understanding to the given options. The correct explanation is that acetylcholine is not degraded, so prolonged depolarization is enforced on the postsynaptic cell.

Key Concepts

Role of Acetylcholinesterase at the Neuromuscular Junction

Acetylcholinesterase is an enzyme that breaks down acetylcholine (ACh) in the synaptic cleft, terminating the signal transmission. Its inhibition leads to accumulation of ACh, causing continuous stimulation of the postsynaptic membrane and prolonged muscle contraction.

Mechanism of Neurotransmission at the Neuromuscular Junction

Neurotransmission involves release of ACh from the presynaptic terminal, binding to receptors on the postsynaptic muscle cell, and triggering depolarization that leads to muscle contraction. Proper degradation of ACh is essential to reset the system for subsequent signals.

Effects of Acetylcholinesterase Inhibitors on Muscle Function

Inhibitors of acetylcholinesterase prevent ACh breakdown, causing excessive stimulation of muscle fibers. This results in prolonged depolarization, muscle fatigue, and potentially paralysis, as the postsynaptic receptors remain activated without normal signal termination.