Botulinum toxin blocks release of which neurotransmitter, leading to flaccid paralysis?

• A. Norepinephrine
• B. Dopamine
• C. Acetylcholine
• D. Gamma-aminobutyric acid

Answer: (C)

Botulinum toxin blocks release of acetylcholine at the neuromuscular junction, leading to flaccid paralysis. Acetylcholine is the chemical signal that tells muscle fibers to contract by binding to nicotinic receptors on the motor end plate. Botulinum toxin acts as a protease that cleaves SNARE proteins necessary for vesicle fusion, so acetylcholine-containing vesicles cannot fuse with the presynaptic membrane and release ACh into the synaptic cleft. Without acetylcholine release, the muscle receives no contractile signal and stays relaxed, producing flaccid paralysis.

Other neurotransmitters aren’t primarily involved in triggering muscle contraction at the neuromuscular junction, so blocking their release wouldn’t produce this effect. For example, norepinephrine and dopamine are mainly involved in autonomic and CNS pathways, and GABA is an inhibitory neurotransmitter in the CNS. (As a contrast, tetanus toxin causes spastic paralysis by blocking inhibitory interneuron signaling in the spinal cord, not by affecting acetylcholine release at the NMJ.)