Figure 6. Pharmacokinetic studies of various drugs affecting NMJ.

(A) A schematic shows the different cellular mechanisms involved in neuromuscular transmission. (B), (C), (D), (E), (F) Dose-dependent responses of coculture contraction frequency exposed to different drugs. (B) Acetylethylcholine mustard hydrochloride blocked the synthesis of acetylcholine (ACh) by irreversibly inhibiting choline acetyltransferase (ChAT). A half maximal inhibitory concentration (IC₅₀) was 1.22 μM. (C) Vesamicol inhibited vesicular acetylcholine transporter (AChT) and prevented filling of synaptic vesicles with ACh. Its IC₅₀ was 98.08 nM. (D) Botulinum toxin A (BoT-A) prevented ACh release by cleaving SNAP-25, a t-SNARE protein essential for fusion of neurotransmitter vesicles with the plasma membrane of motoneuron terminals. Its IC₅₀ was 50.01 pM. (E) Pancuronium blocked neurotransmission by reversibly and competitively binding to acetylcholine receptors (AChRs). Its IC₅₀ was 0.501 μM. (F) Neostigmine increased neuromuscular activities by inhibiting acetylcholinesterase (AChE). Its half maximal effective concentration (EC₅₀) was 0.0461 μM. Quantitative data presented as mean ± SD, n = 6 biological replicates.