NMJ & Muscle Relaxants! Flashcards
Where are ach receptors found on the nmj
ach (nicotinic) receptors are located at the mouths of the junctional folds
what doe junctional folds do at the nmj
increase the surface area
what does ca entry to the pre synaptic nerve terminal do
ca enters via n channels and then ca neutralizes negatively charged membrane which stims fusion and release of NT
Where are a2 receptors located and what is the function of them
located through CNS (mostly pre synaptically) to modulate the release of NT by slowing down deporalization of axon terminal
-used in CNS to decrease central activity
How much ach does each vesical contain
10 000 molecules of ach
what does ach stim do
open up the channels in the endplate to ca,an, k (of only 2 or 3 vesicles hit then a MEPP develops)
How many vessicles for a normal endplate potential of 10-15mmV
200
What is tatanic contraction
no sig reduction in intracellular ca contration so a sustained release results
How does lidocaine work
interferes with sodium channels on the nerve fibres, interfering w the entry of sodium ions preventing firing
What does ethanol do at low and high doeses
at low concentration: may enhance fusion of vesicles
at high concentration: will inhibit the release of ach
what ddoes black widow spider venom do
causes a dramatic and almost complete release of each vesicles from the nerve endings
what does botox do
blocks ach release from vessicles
what do nicotinic antagonists do and what are the 2 classes
block nicotinic channels
- non depolarizing competative blockers
- depolarizing blockers
what are 3 examples of non depolarizing competitive blockers
- D-Tubocurarine
- Pancuronoim + rocurononium
- Atracurium
how do u reverse the effcts of non depolarizing competitive blockers
raise ach conc
-Neostigmine + edrophonium used (achesterase blocers)
