Reduce the leakage of neurotransmitter from the synaptic cleft

Increase the time taken for neurotransmitter to diffuse, allowing finer control of muscle

Increase the surface area from which neurotransmitter could be released

Increase the surface area over which receptors could be located

Reduce the amount of degradation enzymes in the synaptic cleft to break down neurotransmitter

An influx of Mg⁺⁺ into the motor axon terminal

Depolarisation of the muscle membrane adjacent to the motor end plate

An increase in the movement of Na+ and K+ into the motor end plate membrane

Re-uptake of acetylcholine into the motor axon terminal

Binding of acetylcholine to receptors on the motor end plate membrane

Antibodies block the AChR, there are fewer-than-usual vesicles, and there are more AChE molecules

Antibodies block the AChR, there are fewer-than-usual ACh produced, and there are more AChE molecules

Antibodies block the AChR, there is a wider-than-usual synaptic cleft, and there are fewer ACh receptors

Antibodies block the AChR, there are fewer-than-usual Acetyl CoA molecules produced, and there are more AChE molecules

Antibodies block the AChR, there are more AChE molecules, and there are fewer-than-usual Na⁺ and K⁺ ions

The cholinergic AP

The EPP

The APP

The IPSP

The EPSP

SNAP proteins are essential for the release of acetylcholinesterase, which clears up left over acetylcholine allowing for a new action potential to occur

SNAP proteins are essential for the diffusion of acetylcholine across the synaptic cleft to bind onto the motor end plate

SNAP proteins are essential for snapping onto and opening the acetylcholine receptors on the postsyanptic membrane

 SNAP proteins are essential for snapping the vesicles as they leave for exocytosis

 SNAP proteins are essential for docking and fusion of acetylcholine vesicles to the presynaptic membrane

neurotransmitters do not have to be stored in vesicles at the neuromuscular junction

the motor nerve endings secreted noradrenaline

neurotransmitters can be secreted both pre- and post-synaptic terminals

the muscle membrane possesses muscarinic receptors

 the motor nerve endings secrete acetylcholine

Simple diffusion is too fast and would not allow us to control muscle and there are no glial cells at the NMJ for use of uptake mechanisms

Simple diffusion is constrained by the trough design of the NMJ and there are no glial cells at the NMJ for use of uptake mechanisms

Simple diffusion would also cause diffusion of the AChE and glial cells at the NMJ are of the wrong type for re-uptake mechanisms

Simple diffusion would also cause diffusion of the AChE and there are no glial cells at the NMJ for the use of re-uptake mechanisms

Simple diffusion is constrained by the trough design of the NMJ and glial cells at the NMJ do not produce enough AChE