The venom of many cobras contains a potent neurotoxin that binds


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The venom of many cobras contains a potent neurotoxin that binds to ligand-gated Na+ channels, causing them to open. Unlike ACh, which binds to and then rapidly unbinds from ligand-gated Na+ channels, the neurotoxin tends to remain bound to ligand-gated Na+ channels. How does this neurotoxin affect the nervous system’s ability to stimulate skeletal muscle contraction? How does it affect the ability of skeletal muscle fibers to respond to stimulation? I already came up with: When the neurotoxin binds to ligand-gated Na+ channels in the postsynaptic membrane of a skeletal muscle fiber, they open, and Na+ enter the cell, producing graded potentials. When the graded potentials reach threshold, an action potential is produced, stimulating the muscle fiber to contract. However, the neurotoxin tends to remain bound to the ligand-gated Na+ channels, which prevents ACh from binding. Thus, the nervous system’s ability to stimulate the muscle fiber decreases as more and more neurotoxin remain open, Na+ continue to enter the muscle fiver, casuing it s resting membrane potential to depolarize. Eventually, the membrane becomes so depolarized that it is unrepsonsive to stimulation. Death from a cobra bite usually occurs because of parlysis of respiratory muscles. But I need a more in depth answer

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