7 - The Neuromuscular Junction - Vocabulary Flashcards

Key NMJ concepts and terms to memorize for understanding structure, neurotransmission, receptor function, and related diseases.

Neuromuscular Junction (NMJ)

A specialized synapse between a motor neuron and a muscle cell, optimized for rapid, reliable neurotransmission.

Motor endplate

The postsynaptic region of a muscle fiber at the NMJ, with junctional folds and high density of nACh receptors.

End-plate potential (EPP)

Depolarization of the muscle end plate caused by ACh receptor activation, large enough to trigger an action potential in the muscle.

Acetylcholine (ACh)

Neurotransmitter released at the NMJ; binds to nicotinic ACh receptors to cause depolarization.

Acetylcholinesterase (AChE)

Enzyme that hydrolyzes ACh in the synaptic cleft to terminate signaling.

Nicotinic acetylcholine receptor (nAChR)

Ligand-gated ion channel on the end plate permeable to Na+ and K+, activated by ACh.

Ionotropic receptor

A ligand-gated ion channel; example: nAChR at the NMJ.

Transverse (T) tubules

Membrane invaginations that carry action potentials deep into the muscle fiber.

DHP receptor (L-type Ca2+ channel)

Voltage-gated Ca2+ channel in T-tubules that senses depolarization to trigger Ca2+ release from the SR.

Ryanodine receptor (RyR)

Ca2+ release channel on the sarcoplasmic reticulum activated during excitation-contraction coupling.

Ca2+ influx (presynaptic)

Ca2+ entry through voltage-gated channels that triggers vesicle fusion and ACh release.

Synaptotagmin

Ca2+ sensor that triggers vesicle fusion when Ca2+ binds.

Vesicle exocytosis

Release of acetylcholine from presynaptic vesicles into the synaptic cleft.

Quanta

Discrete packets of neurotransmitter released from presynaptic vesicles; multiple quanta per NMJ event.

Fate of acetylcholine (ACh)

ACh is released into the cleft and hydrolyzed by AChE, terminating the signal.

End-plate potential (EPP) amplitude

Typically about -20 mV at the end plate; decays with distance from the NMJ.

Junctional folds

Postsynaptic membrane infoldings that increase receptor density and Na+ channel density.

Myasthenia gravis

Autoimmune disease reducing nAChR density at the NMJ, causing muscle weakness; treated with AChE inhibitors such as neostigmine.

Excitation-contraction coupling (ECC)

Process by which an action potential leads to muscle contraction via Ca2+ release from the SR.