Neuromuscular blocking agents and transmembrane potential gradients
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1. A certain type of poison is a nicotinic receptor blocker. What affect would this poison have on the muscle action potential?
2. Some inhibitory postsynaptic potentials (IPSPs) are the result of Cl- entering the cell through a chloride channel. Other IPSPs are caused by the opening of K+ channels. How could movement of the potassium ion result in hyperpolarization of the postsynaptic cell.
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Solution Summary
Agents that inhibit the nicotinic acetylcholine receptor prevent binding of the normal ligand, acetylcholine. This blocking effect prevents channel opening and the formation of EPSPs. Loss of potassium ions from the cell interior, in the absence of an influx of sodium ions or accompanying loss of interior negatively charged chloride ions, results in an even greater interior negative potential: hyperpolarization.
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1. "Poisoning" of the nicotinic receptor implies a neuromuscular blocking agent, specific for the nicotinic acetylcholine receptor. These agents are very common in anesthesia practice, e.g., pancuronium, vecuronium, curare. Also, some neurotoxins, for instance the cone snail toxins termed conotoxins and α-bungarotoxin, toxin of the banded krait snake, block nicotinic ...
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