EXCITATION CONTRACTION COUPLING

Where do the motor neurons that activate skeletal muscle reside?

Brainstem & spinal cord (somatic motor neurons).

What initiates neurotransmitter release at the axon terminal?

-Arrival of neuron AP →

-Opening of voltage-gated Ca²⁺ channels →

-Ca²⁺ influx.

What neurotransmitter is released at all skeletal neuromuscular junctions?

Acetylcholine (ACh).

What kind of channel is the nicotinic ACh receptor at the motor end plate?

Ligand-gated cation channel (chemically gated), permeable to Na⁺ & K⁺.

Why does ACh receptor activation depolarize the end plate?

It passes more Na⁺ in than K⁺ out → net positive influx → end-plate potential.

Is the end-plate potential graded or all-or-none?

Graded (local); it can summate to reach threshold in adjacent sarcolemma.

What opens the voltage-gated Na⁺ channels in the sarcolemma?

Reaching threshold due to the EPP spreading to adjacent membrane.

After initiation, where does the muscle AP propagate?

Along the sarcolemma & down the T-tubules.

Define the triad in skeletal muscle.

Terminal cisterna – T-tubule – terminal cisterna

At the A-band/I-band junction.

Primary function of the terminal cisternae?

Store Ca²⁺ & release it rapidly during excitation.

What event triggers Ca²⁺ release from the SR terminal cisternae?

T-tubule depolarization couples to SR Ca²⁺ channels → they open.

Immediate molecular target of Ca²⁺ to initiate contraction?

Troponin (troponin-C subunit binds Ca²⁺).

What happens to tropomyosin when Ca²⁺ binds troponin?

It shifts off actin’s myosin-binding sites, exposing them.

What forms a cross-bridge?

Myosin head binding to an exposed site on actin.

What biochemical state of myosin is “cocked” & ready to bind actin?

Myosin-ADP-Pi (after ATP hydrolysis).

What directly causes the power stroke?

Release of Pi (& then ADP) from the myosin head after actin binding.

What causes myosin to detach from actin?

Binding of a new ATP to the myosin head.

What re-cocks (re-primes) the myosin head?

Hydrolysis of the newly bound ATP → ADP + Pi.

What terminates contraction?

Ca²⁺ reuptake into SR by SERCA pumps → Ca²⁺ dissociates from troponin.

Why is ATP required during relaxation as well?

-SERCA pumps use ATP to move Ca²⁺ back into SR;

-ATP also needed for myosin detachment.

Where exactly is the NMJ specialization on the muscle fiber?

Motor end plate with junctional folds to increase receptor density/area.

What distinguishes EPP from a muscle AP in terms of channels?

-EPP uses ACh receptor (ligand-gated);

-AP uses voltage-gated Na⁺/K⁺ channels.

What ensures rapid, uniform activation of each sarcomere?

Triads at A-I junction around each sarcomere → synchronized Ca²⁺ release.

Saltatory conduction occurs in which cell & why?

The motor neuron axon due to myelination (nodes of Ranvier).

What happens to ACh after it’s released?

It’s quickly broken down by acetylcholinesterase to terminate the signal.

What happens if ATP is absent?

Myosin cannot detach → rigor (rigor mortis post-mortem).

What ion movement defines threshold at the sarcolemma?

Sufficient Na⁺ influx (via voltage-gated Na⁺ channels) to trigger the AP.

Source of Ca²⁺ for contraction in skeletal muscle vs. cardiac?

Skeletal: SR (terminal cisternae);

Cardiac: SR & extracellular Ca²⁺ via L-type channels (contrast point).