Over time, the motor end plate is destroyed.

Since the motor end plate is depolarized, further signals to contract have no effect (paralysis).

The area where the nerve contacts the muscle is called the neuromuscular junction, or the motor end plate.

Maybe a muscle-tissue extract would be better than a serum sample, since the toxin is active on motor end plates.

It acts on nicotinic receptors resulting in persistent depolarization of the motor end plate.

Regeneration of the motor end plates will occur, as long as the endoneural tubules are intact.

The alpha motoneuron communicates with acetylcholine receptors on the motor end plate of the effector muscle.

A regional lightweight women's power lifting champion with microprocessors implanted in the motor end plates of muscles in thighs and back.

Reception of acetylcholine neurotransmitters on the motor end plate causes contraction of that effector muscle.

That would give an initial jolt as if you injected a bolus of acetylcholine into all the ganglionic synapses and motor end plates.

A neuromuscular non-depolarizing agent is a form of neuromuscular blocker that does not depolarize the motor end plate.

Scientists agree thyroxine brings about the degradation of muscle fibers specifically at the motor end plates of neuromuscular junctions.

Vecuronium operates by competing for the cholinoceptors at the motor end plate thereby exerting its muscle-relaxing properties which are used adjunctively to general anesthesia.

Acetylcholine diffuses into the synaptic cleft and can bind to the nicotinic acetylcholine receptors on the motor end plate.

It may be hydrolysed by acetylcholine esterase (AchE) or bind to the nicotinic receptors located on the motor end plate.

Depolarisation of the motor end plate causes potassium ions to leave the muscle cells, repolarising the muscle and closing the calcium channels.

The intracellular microelectrode monitored the amplitude of the depolarization of the motor end plate in response to ACh binding to nicotinic (ionotropic) receptors.

Botulinum toxin type A is most often used; it prevents the release of acetylcholine from the presynaptic axon of the motor end plate, paralyzing the dystonic muscle.

The toxin goes straight to nerve endings, or motor end plates, and blocks the normal release of acetylcholine, a natural chemical that transmits nerve impulses to help muscles contract.

The ability of acetylcholine receptors to increase and decrease in number on the motor end plate of the effector muscle represents the post-synaptic plasticity of the motor unit.

If repeated impulses are administered (two per second or 2 Hz), it is normal for CMAP amplitudes to become smaller as the acetylcholine in the motor end plate is depleted.

The axon terminal depolarizes and releases Acetylcholine (ACh), a neurotransmitter, which in turn stimulates the motor end plate (MEP) of the muscle fiber the nerve is innervating.

After the threshold stimulus is reached, protein receptors in the motor end plate detect the neurotransmitter and an impulse spreads over the sarcolemma and into the T-tubules, where it goes to the sarcoplasmic reticulum.

In MG, the autoantibodies most commonly act against the nicotinic acetylcholine receptor (nAChR), the receptor in the motor end plate for the neurotransmitter acetylcholine that stimulates muscular contractions.

Acetylcholinesterase inhibitors: neostigmine and pyridostigmine can improve muscle function by slowing the natural enzyme cholinesterase that degrades acetylcholine in the motor end plate; the neurotransmitter is therefore around longer to stimulate its receptor.