The neuromuscular junction (NMJ) is the site responsible for impulse transmission between nerve endings and muscle fibers. This process requires the release of acetylcholine (ACh) from the presynaptic membrane and its binding to the acetylcholine receptor (AChR) on the postsynaptic membrane. Under normal physiological conditions, when the action potential reaches the motor nerve endings, the voltage-gated calcium ion channels are activated, causing calcium ions to flow into the nerve endings. Subsequently, synaptic vesicles containing ACh are released from the presynaptic membrane [1]. The spontaneous release of synaptic vesicles produces miniature end-plate potentials (mEPPs). During nerve impulses, the synchronous release of many synaptic vesicles leads to a large-scale depolarization of the end-plate membrane, and the addition of miniature end-plate potentials produces end-plate potentials (EPPs). When the peak of Epps reaches the critical threshold, it will trigger the action potential (AP) in the muscle fibers. In normal muscles, this series of events will occur in each nerve impulse. The binding of ACh to the receptor on the postsynaptic membrane opens the ACh cation-specific channel, causing local depolarization and activating adjacent voltage-gated sodium channels. This process converts chemical signals into electrical signals, i.e., the AP of muscle fibers. The role of acetylcholinesterase in the hydrolysis of ACh is crucial, which can prevent a single ACh molecule from repeatedly activating AChR. The effective nerve transmission of the neuromuscular junction originates from the amount of ACh released into the synapse being higher than the amount required to trigger the AP, thus maintaining long-term repetitive muscle fiber contraction [1, 2]. The part of the EPPs amplitude that exceeds the amplitude required to trigger the AP is called the “safety factor” [3]. The term “safety factor” is used to describe the effectiveness of NMJ transmission, specifically defined as the ratio between the actual neurotransmitter release produced by the nerve and the amount of neurotransmitter required to trigger the AP [3]. Factors affecting the safety factor of NMJ include the amount of ACh release, the density of AChR at the postsynaptic membrane and secondary postsynaptic membrane folds, and the density of sodium ion channels [2]. The density of AChR and sodium ion channels at the postsynaptic membrane folds depends on the presence of postsynaptic membrane folds, which determine the density of voltage-gated sodium channels in the postsynaptic membrane, thereby increasing the effective coupling of local EPPs and muscle fiber action potentials [2].