Answer:
At the neuromuscular junction, calcium must enter the synaptic end bulb to stimulate the release of acetylcholine, which binds to ligand gates so sodium ions can enter the muscle fiber.
Explanation:
Skeletal fiber contractions are based on different physiological and biochemical phenomena that happen in every cell. These phenomena are due to stimulation produced by somatic motor neurons, which axons get in contact with muscle fibers through a neuromuscular synapse. In rest, attraction strengths between myosin and actin filaments are inhibited by the tropomyosin. When an action potential is originated in the central nervous system, it travels to the somatic motor neuron membrane: the muscle fiber, and activates the calcium channels releasing it in the neuron. Calcium makes vesicles to fuse with the membrane and release the neurotransmitter named acetylcholine (Ach) into the synaptic space in the juncture. Then, Ach binds to its receptors on the skeletal muscle fiber. This causes the ion channels to open, and positively charged sodium ions cross the membrane to get into the muscle fiber (sarcoplasm) and potassium get out. The difference in charges caused by the migration of sodium and potassium makes the muscle fiber membrane to become more positively charged (depolarized). The action potential caused by this depolarization enters the t-tubules depolarizing the inner portion of the muscle fiber. This activates calcium channels in the T tubules membrane, that make the calcium be released into the sarcolemma. At this point, tropomyosin is obstructing binding sites for myosin on the thin filament. When calcium binds to the troponin C, the troponin T alters the tropomyosin by moving it and then unblocks the binding sites. Myosin binds to the uncovered actin-binding sites, and while doing it ATP is transformed into ADP and inorganic phosphate. Z-bands are then pulled toward each other, thus shortening the sarcomere and the I-band, and producing muscle fiber contraction.
