The Neuromuscular Junction Flashcards
DHP vs Ryanodine channels
DHP channels are on T-tubules and receive the action potential. Open and transmits signal to the ryanodine receptors via calcium
Ryanodine receptors are on sarcoplasmic reticulum and release the calcium into the muscle cells where it then binds to troponin and allows contraction
What channel does muscle use to get calcium out of cells?
ATP via receptors on sarcoplamic reticulum and the sodium/calcium exchanger on the outside of the cell.
Sympathetic vs parasympathetic neurotransmitter release
Sympathetic always norepinephrine that binds to adrenergic receptors (a or b)
Parasympathetic always acetylcholine (
Difference between skeletal and cardiac muscle
Cardiac all fire together when stimulated, skeletal muscle does not
Calmodulin
Molecule that acts similar to troponin but in smooth muscle.
Binds calcium released by sarcoplasmic reticulum and activates MLCK
Two ions involved in generating action potentials
Calcium and sodium
What two ions conductance are present in the action potential?
Sodium and potassium
- potassium’s peak conductance is in the refractory period
- sodium’s peak conductance is in the peak of the action potential
Do gradients change when ions move in the body as it pertains to action potentials?
NO
- only changes due to physiological issues such as trauma or renal dysfunction
What happens at the beginning of the action potential? P
Both sodium and potassium channels open
- sodium hits peak conductance quicker since they are faster channels but also reduces conductance quicker
- potassium is slower conductance but takes longer to close (refractory period)
Activation and inactivation gates of sodium
At rest: inactivation gate is open and activation is closed
Nerve impulse reaches cell: both gates are open
After impulse is gone: inactivation gate is closed and activation gate is open
Sodium is faster because it has 2 channels
What happens to resting membrane potential during hyperkalemia?
Increases because the gradient of potassium decreases
Actually does not increase chance of firing from action potential because small positive changes in resting membrane potentials close inactivation gates in sodium channels
This is why hyperkalemia is bad
Steps of NMJ activation in skeletal muscle
1) action potential reaches presynaptic neuron synapse
2) voltage gated calcium channels open and allow calcium in
3) ACh vesicles are released in response to high intracellular calcium
4) ACh binds to cholinergic nicotinic receptors on postsynaptic neuron
5) ligand gated channel opens with sodium into the motor end plate and potassium out of cell
- sodium has a huge gradient so it moves in quicker
6) sodium depolarizers motor end plate and propagates action potential down the motor end plate.
What toxins block potassium channels
Dendrotoxin
What toxins disable ACh release by cleaving SNAREs
Tetanus toxin and Botulism toxin
What toxins disable sodium channels?
Tetrodotoxin and saxitoxin
