The acetylcholine receptors are similar to those in smooth muscle.
The nerve ending contains many vesicles and mitochondria.
Lack of Ca diminishes the release of acetylcholine.
There is a high concentration of the cholinesterase enzyme.
There is a delay of neuromuscular transmission of 0.5 millisecond
Neuromuscular transmission occurs only from the muscle to the nerve.
EPP is always maximal and rapidly conducted along the surface of the muscle.
EPP is a localized state of depolarization at the motor end plate.
EPP is augmented by increased Mg concentration in ECF.
EPP is associated with decreased excitability of the motor end plate.
The resting membrane potential is about -90 mV.
The magnitude of the action potential is more than that in nerves.
The firing level is reached after about +40 mV of depolarization.
The spike is propagated along the muscle surface at a speed of 5 m /second.
Has a prolonged plateau phase.
Has a smaller magnitude than that of smooth muscles.
Causes uptake of Ca into the lateral sacs of the sarcoplasmic reticulum.
Spreads inwards to all parts of the muscle fibre via the T-tubules.
Is not essential for contraction.
Is caused by release of acetylcholine from the muscle side.
Shows a permeability change to Na+ at the receptor side of the neuro-muscular junction
Can be facilitated by curare.
Is blocked by curare because it competes with Na+ influx at the M.E.P.
Ca++ enters through synaptic cleft.
Ach is released from synaptic cleft.
There is a delay of about 5 milliseconds.
The impulse is transmitted in one direction.