In depolarizing one why did the sodium gates remain opened and if sodium influx takes place then intracellular membrane potential will be positive so how did the persistent depolarisation will take place While in non depolarizing one you told that drug will block the binding of ach along with closing of sodium gates
Depolarizing nmb's are the agonist bind with receptor and sodium channel gets open and sodium influx take place.Intra cellular charge become possitive.Then how skeletal muscle relaxation take place. Ach also depolarize cell. How its happen?
Suxamethonium is a compount of two acetylcholine molecules joined back-to-back which causes a prolonged depolarisation of the neuromuscular junction to a membrane potential above which action potential cannot be triggered. Normal neural transmission of action potential through indigenous acetylcholine stores does not happen hence an initial depolarisation (usually manifested by fasciculations) then followed by paralysis.
Hello! SRNA here! We are currently learning that one of the mechanisms behind the decreasing amplitude in TOF twitches has to do with the NDMR blocking a n-ACh-R auto-receptor on the motor neuron. This blocking inhibits the movement of VP1 ACh vesicles to VP2 position thereby decreasing the amount of ACh released with each impulse. Here in the video it is saying that the NDMR is blocking ChT (Choline transporter) and blocking the uptake of choline into the cell, thereby decreasing the actual production of ACh. Just wondering if you can tell me which is correct or maybe it is a combination of the two?
Wow this was so easy to understand! You literally made medicine so much more interesting 🔥
Glad you liked it!
This was such a great explanation! Thank you.
In depolarizing one why did the sodium gates remain opened and if sodium influx takes place then intracellular membrane potential will be positive so how did the persistent depolarisation will take place
While in non depolarizing one you told that drug will block the binding of ach along with closing of sodium gates
Cu respect din Romania Domnul Isus sa va binecuvanteze Amin
Depolarizing nmb's are the agonist bind with receptor and sodium channel gets open and sodium influx take place.Intra cellular charge become possitive.Then how skeletal muscle relaxation take place. Ach also depolarize cell. How its happen?
Suxamethonium is a compount of two acetylcholine molecules joined back-to-back which causes a prolonged depolarisation of the neuromuscular junction to a membrane potential above which action potential cannot be triggered. Normal neural transmission of action potential through indigenous acetylcholine stores does not happen hence an initial depolarisation (usually manifested by fasciculations) then followed by paralysis.
Was part 3 ever made? I cannot find the video about the antidotes.
honestly very well made and explained
Hello! SRNA here! We are currently learning that one of the mechanisms behind the decreasing amplitude in TOF twitches has to do with the NDMR blocking a n-ACh-R auto-receptor on the motor neuron. This blocking inhibits the movement of VP1 ACh vesicles to VP2 position thereby decreasing the amount of ACh released with each impulse. Here in the video it is saying that the NDMR is blocking ChT (Choline transporter) and blocking the uptake of choline into the cell, thereby decreasing the actual production of ACh. Just wondering if you can tell me which is correct or maybe it is a combination of the two?
Why depolarizing neuromuscular agent act on post synaptic and
Non depolarizing act on pre synaptic
Very helpful, thank a lot
Blessing this is amazing
Very helpful
Great video!
Thanks a lot 🥺💗
thank you
BEST❣️
Thank u
Great, ty
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