After death, the consumption of ATP continues but the generation stops. Therefore in the absence of ATP, actin and myosin filaments become permanently complexed and rigor mortis sets in (Raff, 290).
2. During surgery, anesthetics are administered to patients blocking the action potential generation. These anesthetics target the function of voltage-gated sodium channels. Local anesthetics work by blocking the entry of sodium ions into their channels therefore preventing transient increase in permeability of the nerve membrane to sodium ions into their channels thereby preventing the transient increase in permeability of the nerve membrane to sodium ions for generating action potential.
Binding of both protonated and neural local anesthetic molecules interferes with conformational changes that underlie the process of channel activation. The failure of sodium ion channel permeability to increase slows own the rate of depolarization since an action potential is not propagated. This interferes with nerve transmission since failure in action potential will cause inability of flow of current from depolarized sites inside surface of the cell membrane to adjacent polarized membrane (Raff, 170).
3. People with Alzheimer’s disease are forgetful and with disease progression they become confused and lose their ability to speak. These patients often have diminished acetylcholine transferase activity in their brains. The enzyme that synthesizes acetylcholine by transferring the acetyl group from acetyl-coA to choline. Acetylcholine is a major neurotransmitter in the nervous system. It is produced in cholinergic neurons from choline and acetyl co enzyme A by action of acetyltransferase. Acetylcholine is stored in vesicles at the presynaptic cell terminal and released after excitation. After acetylcholine is released into the synapse, it is broken down into smaller parts and taken up by the nerves so that it can be reused. Decrease of acetylcholine in the