Final answer:
Succinylcholine's effects at the neuromuscular junction are terminated by acetylcholinesterase, which degrades the neurotransmitter acetylcholine, ending muscle contraction.
Step-by-step explanation:
The termination of the effects of succinylcholine at the neuromuscular junction occurs as a result of the enzyme acetylcholinesterase (AChE), which breaks down the neurotransmitter acetylcholine (ACh) in the synaptic cleft. This degradation of ACh prevents it from rebinding to the receptors on the muscle cell, terminating the signal that causes muscle contraction.
Since succinylcholine acts as a depolarizing neuromuscular blocker mimicking ACh, its action is also terminated by AChE. Thus, muscle relaxation occurs as AChE degrades both ACh and succinylcholine within the neuromuscular junction, allowing the muscle fiber to repolarize and return to its resting state.