When experimentally applying alpha-bungarotoxin to a muscle,you find that it does not contract when the motor neuron leading to it is electrically stimulated.Knowing that this toxin blocks acetylcholine receptors,what can you conclude about the failure to contract?
A)A contraction fails to occur because this toxin prevents cross-bridge formation and thereby directly prevents contraction.
B)A contraction fails to occur because acetylcholine is not released from the motor neuron.
C)A contraction fails to occur because this toxin directly prevents calcium ion release from intracellular stores.
D)A contraction fails to occur because an action potential is not generated in the muscle cell.
E)A contraction fails to occur because neurotransmitter release by the motor neuron is blocked at the neuromuscular junction.

Question

Quizplus · Accepted Answer

Alpha-bungarotoxin blocks acetylcholine receptors at the neuromuscular junction, preventing acetylcholine from binding to its receptors on the muscle cell. This blockade means that the normal depolarization of the muscle cell membrane, which is necessary to trigger an action potential leading to muscle contraction, cannot occur. The toxin does not directly affect neurotransmitter release, cross-bridge formation, or calcium ion release; it specifically prevents the initiation of an action potential in the muscle cell by blocking acetylcholine receptors.

When Experimentally Applying Alpha-Bungarotoxin to a Muscle,you Find That It