<prompt> Please answer with one of the option in the bracket. Write reasoning in between . Write answer in between .Q:A well-dressed couple presents to the emergency department with sudden onset of headache, a sensation of floating, and weakness of arms and legs after eating a plate of shellfish 2 hours ago. They mention that they had experienced tingling of the lips and mouth within 15 minutes of ingesting the shellfish. They also complain of mild nausea and abdominal discomfort. On physical examination, their vital signs are within normal limits. Their neurological examination reveals decreased strength in all extremities bilaterally and hyporeflexia. After detailed laboratory evaluation, the physician confirms the diagnosis of paralysis due to the presence of a specific toxin in the shellfish they had consumed. Which of the following mechanisms best explains the action of the toxin these patients had consumed?? A: Inactivation of synaptobrevin, B: Inactivation of syntaxin, C: Blockade of voltage-gated fast sodium channels, D: Increased opening of presynaptic calcium channels, E: Inhibition of acetylcholinesterase,  <response>: This is a clinical vignette describing a couple who developed acute neurological symptoms after eating shellfish. The key findings are tingling of the lips and mouth shortly after ingesting the shellfish, followed by headache, weakness, and hyporeflexia, indicating a paralytic condition likely due to a toxin in the shellfish. The question asks about the mechanism of action of the toxin. Based on the acute onset after shellfish ingestion and the neurological findings, this is most likely a case of shellfish poisoning, either paralytic shellfish poisoning PSP or neurotoxic shellfish poisoning NSP. PSP is caused by saxitoxins which block voltage-gated sodium channels. NSP is caused by brevetoxins which activate voltage-gated sodium channels. Both mechanisms result in disruption of nerve conduction and paralysis.Of the choices given, blockade of voltage-gated sodium channels best explains the neurological deficits seen in this case.C: Blockade of voltage-gated fast sodium channels 