What is the motor endplate?
The specialized postsynaptic region of a muscle cell. The motor endplate is immediately across the synaptic cleft from the presynaptic axon terminal. Among its anatomical specializations are junctional folds which harbor a high density of cholinergic receptors.
Is motor end plate a synapse?
Neuromuscular junctions, also called motor end plates, are specialised chemical synapses formed at the sites where the terminal branches of the axon of a motor neuron contact a target muscle cell.
What is motor end plate in neuromuscular junction?
Motor End Plate forms the postsynaptic part of NMJ. It is the thickened portion of the muscle plasma membrane (sarcolemma) that is folded to form depressions called junctional folds. The terminal nerve endings do not penetrate the motor endplate but fit into the junctional folds.
What happens at the motor end plate?
Mechanism of action. Botulinum toxin’s effects occur at the motor end plate. Muscle contraction occurs when motor nerve terminal impulse reaches a nerve ending, which in turn releases acetylcholine across the neuromuscular gap to the muscle signaling muscle contraction.
Is broken down by acetylcholinesterase?
Acetylcholinesterase (AChE) is a cholinergic enzyme primarily found at postsynaptic neuromuscular junctions, especially in muscles and nerves. It immediately breaks down or hydrolyzes acetylcholine (ACh), a naturally occurring neurotransmitter, into acetic acid and choline.
Can minis be blocked by curare?
Amplitude of MEPPs This answer is CORRECT! Curare is a competitive inhibitor of ACh, hence it will inhibit or reduce the amplitude of the miniature end-plate potential.
What would happen if acetylcholine was not removed from the synaptic cleft?
What would happen if acetylcholine was not removed from the synaptic cleft? Multiple action potentials would occur in the muscle fiber.
What is the final trigger for muscle contraction?
Muscle contraction usually stops when signaling from the motor neuron ends, which repolarizes the sarcolemma and T-tubules, and closes the voltage-gated calcium channels in the SR. Ca++ ions are then pumped back into the SR, which causes the tropomyosin to reshield (or re-cover) the binding sites on the actin strands.