Tubocurarine competitively antagonizes nAchR. Phrenic nerve was still functioning, so the problem was at the neuromuscular junction. Of the answer choices, the only pure NMJ blocker was this
solidshakeJust to show why the other answers are wrong: Lidocaine - Blocks Na channels, Morphine Sulfate - mu opioid receptor blocker, Pentobarbitol - increased duration of GABA-A channel thus increased Cl thus decreased nerve firing, Potassium Chloride - replenish K, Tetrodotoxin - Blocks Na channels. Question shows Phrenic nerve trying to make the diaphram move with Ach release but fails because Tubocurarine is a competitive antagonist of Ach at the NMJ. +8
ythotuboCURARine, from root word CURARE (plant extract historically used in poison arrows) -aloha+
wherearetheanswersI get why tubocurarine would cause this, but can someone explain why it also couldn't be tetrodotoxin?+1
wherearetheanswersActually some googling helped! In case anyone else is wondering, tubocurarine acts at the NMJ so you would get continued phrenic nerve depolarization like you see in the figure. Conversely, tetrodotoxin works at sodium channels which are on axons so blockade of this would result in decreased phrenic nerve activity as well. +8
submitted by โkevin(52)
Tubocurarine competitively antagonizes nAchR. Phrenic nerve was still functioning, so the problem was at the neuromuscular junction. Of the answer choices, the only pure NMJ blocker was this