How does succinylcholine cause muscle paralysis?
Succinylcholine causes a flaccid paralysis by binding to the acetylcholine (nicotinic) receptor at the neuromuscular junction. When acetylcholine binds this receptor, it triggers the opening of sodium channels that are connected to the receptor. Sodium rushes into the cell, raising the membrane voltage in the cytoplasm just next to the NMJ. This small rise in membrane voltage triggers a second set of sodium channels to open, which rapidly depolarize the whole cell. This depolarization is the signal for muscle contraction. By the time contraction begins, the sodium channels have closed, and the cell has returned to resting membrane potential. When succinylcholine binds the nicotinic receptor, it triggers opening of the first set of sodium channels, same as with acetylcholine. However, unlike acetylcholine, it does not allow the channels to close after the cell has depolarized. This means that sodium can continually flood the cell, and disrupt the cycle of depolarization-repolarization, and prevent muscle contraction from taking place.
How is the energy harvested from the oxidation of acetyl-CoA in the TCA cycle linked to the production of ATP?
When acetyl-CoA is broken down, energy is harvested by NAD+ and FAD+ in the form of high-energy electrons. These two molecules work to deliver the electrons, and their energy, to the electron transport chain, where they are used to indirectly power ATP synthase, the enzyme responsible for synthesizing ATP.
Which adductor of the hip joint receives its innervation from two major nerves, and what are those nerves?
Adductor magnus is innervated by both the obturator nerve and the tibial division of the sciatic nerve.