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QUESTION:

Apply What You Have Learned

Botulinum neurotoxin blocks exocytosis (release) of ACh at the neuromuscular junction. As a result, which of the following events cannot occur?

Formation of an end-plate potential.

What would happen if, during crossbridge cycling, ATP "ran out" but sarcoplasmic calcium concentration remained high?
Select all that apply.

  • The myosin heads would be unable to detach from actin.
  • The muscle cell would be unable to relax.

Structure of a Neuromuscular Junction and Skeletal Muscle Fiber

Correctly labelled image from phase 1. Select enter or spacebar for full description.

Structures Associated With Excitation-Contraction Coupling

Correctly labelled image from phase 3. Select enter or spacebar for full description.

Structure and Arrangement of Thick and Thin Filaments

Correctly labelled image from phase 5. Select enter or spacebar for full description.

Summary

Correctly labelled image from phase 7. Select enter or spacebar for full description.

Recap

Critical Concepts

Excitation of a Skeletal Muscle Cell

  • Skeletal muscle contraction is initiated by a motor neuron.
  • A nerve impulse (action potential) is propagated along the motor neuron to a neuromuscular junction (NMJ) with a skeletal muscle fiber.

The Axon Terminal

  • Arrival of an action potential at the synaptic knob causes voltage-gated calcium (Ca2+) channels to open.
  • Ca2+ diffuses into the synaptic knob where it binds to synaptic vesicles, initiating exocytosis of neurotransmitter acetylcholine (ACh) into the synaptic cleft.
  • ACh diffuses across the synaptic cleft, binding to ligand-gated channels (ACh receptors). Each ACh receptor binds two ACh molecules to open, but only one binding site is shown here.
  • Sodium (Na+) diffuses into the muscle cell.
  • This results in a small, localized depolarization called the end-plate potential (EPP). The EPP spreads away from the NMJ.

Sarcolemma and T-tubules

  • The end-plate potential causes voltage-gated channels near the NMJ to reach threshold, generating an action potential (AP) that propagates across the sarcolemma.
  • The network of T-tubules and sarcoplasmic reticulum ensures all myofibrils respond in unison.
  • At the triad, an action potential travels down the T-tubule.
  • Voltage-sensitive receptors initiate the opening of calcium channels in the sarcoplasmic reticulum (SR).
  • Ca2+ diffuses out of the SR and into the sarcoplasm.

Structure of a Sarcomere

  • The sarcomere contains a highly organized array of overlapping thick and thin filaments, stabilized by additional structural supports including the M-line and Z-discs.

Interactions Between Thick and Thin Filaments Result in Contraction

  • A sarcomere contains a highly organized array of overlapping thick and thin filaments.

Energizing the Myosin Head

  • Myosin heads project outward from the thick filament toward the thin filament.
  • The myosin head can hydrolyze ATP, causing a conformation (shape) change to the energized state.

Crossbridge Formation

  • Troponin and tropomyosin are regulatory proteins associated with actin of thin filaments.
  • Calcium released from the SR binds to troponin, causing a conformational change in troponin and tropomyosin, exposing the myosin binding sites on actin.

Crossbridge Formation and Power Stroke

  • Myosin heads form crossbridges as they bind to the newly exposed binding sites on actin.
  • Binding to actin causes myosin heads to pivot, pulling actin toward the center of the sarcomere; this is the power stroke.
  • Binding of another ATP allows release of myosin from actin, and ATP hydrolysis energizes myosin heads so the crossbridge cycle can repeat.

Crossbridge Cycling

  • Crossbridge cycling continues as long as calcium and ATP are present.
  • Each cycle slides thin filaments further toward the center of the sarcomere; Z discs are pulled along and the entire sarcomere shortens.

Overview of Contraction

  • Coordinated contraction of sarcomeres ultimately produces shortening of the entire muscle.

ANSWER:

Apply What You Have Learned

Botulinum neurotoxin blocks exocytosis (release) of ACh at the neuromuscular junction. As a result, which of the following events cannot occur?

Formation of an end-plate potential.

What would happen if, during crossbridge cycling, ATP "ran out" but sarcoplasmic calcium concentration remained high?
Select all that apply.

  • The myosin heads would be unable to detach from actin.
  • The muscle cell would be unable to relax.

Structure of a Neuromuscular Junction and Skeletal Muscle Fiber

Correctly labelled image from phase 1. Select enter or spacebar for full description.

Structures Associated With Excitation-Contraction Coupling

Correctly labelled image from phase 3. Select enter or spacebar for full description.

Structure and Arrangement of Thick and Thin Filaments

Correctly labelled image from phase 5. Select enter or spacebar for full description.

Summary

Correctly labelled image from phase 7. Select enter or spacebar for full description.

Recap

Critical Concepts

Excitation of a Skeletal Muscle Cell

  • Skeletal muscle contraction is initiated by a motor neuron.
  • A nerve impulse (action potential) is propagated along the motor neuron to a neuromuscular junction (NMJ) with a skeletal muscle fiber.

The Axon Terminal

  • Arrival of an action potential at the synaptic knob causes voltage-gated calcium (Ca2+) channels to open.
  • Ca2+ diffuses into the synaptic knob where it binds to synaptic vesicles, initiating exocytosis of neurotransmitter acetylcholine (ACh) into the synaptic cleft.
  • ACh diffuses across the synaptic cleft, binding to ligand-gated channels (ACh receptors). Each ACh receptor binds two ACh molecules to open, but only one binding site is shown here.
  • Sodium (Na+) diffuses into the muscle cell.
  • This results in a small, localized depolarization called the end-plate potential (EPP). The EPP spreads away from the NMJ.

Sarcolemma and T-tubules

  • The end-plate potential causes voltage-gated channels near the NMJ to reach threshold, generating an action potential (AP) that propagates across the sarcolemma.
  • The network of T-tubules and sarcoplasmic reticulum ensures all myofibrils respond in unison.
  • At the triad, an action potential travels down the T-tubule.
  • Voltage-sensitive receptors initiate the opening of calcium channels in the sarcoplasmic reticulum (SR).
  • Ca2+ diffuses out of the SR and into the sarcoplasm.

Structure of a Sarcomere

  • The sarcomere contains a highly organized array of overlapping thick and thin filaments, stabilized by additional structural supports including the M-line and Z-discs.

Interactions Between Thick and Thin Filaments Result in Contraction

  • A sarcomere contains a highly organized array of overlapping thick and thin filaments.

Energizing the Myosin Head

  • Myosin heads project outward from the thick filament toward the thin filament.
  • The myosin head can hydrolyze ATP, causing a conformation (shape) change to the energized state.

Crossbridge Formation

  • Troponin and tropomyosin are regulatory proteins associated with actin of thin filaments.
  • Calcium released from the SR binds to troponin, causing a conformational change in troponin and tropomyosin, exposing the myosin binding sites on actin.

Crossbridge Formation and Power Stroke

  • Myosin heads form crossbridges as they bind to the newly exposed binding sites on actin.
  • Binding to actin causes myosin heads to pivot, pulling actin toward the center of the sarcomere; this is the power stroke.
  • Binding of another ATP allows release of myosin from actin, and ATP hydrolysis energizes myosin heads so the crossbridge cycle can repeat.

Crossbridge Cycling

  • Crossbridge cycling continues as long as calcium and ATP are present.
  • Each cycle slides thin filaments further toward the center of the sarcomere; Z discs are pulled along and the entire sarcomere shortens.

Overview of Contraction

  • Coordinated contraction of sarcomeres ultimately produces shortening of the entire muscle.

Posted by Cleveland on February 24, 2026
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