Due MIDNIGHT: Respond/Critique two discussion posts.

The action potential of a neuron begins when voltage-gated channels open due to reaching their threshhold value (McKinley 2013). Once this occurs, the charges between the inside and outside of the neuron plus the traveling of chemicals is able to be exchanged. For example, if there is a substantial amount of Na+ within the cell, the opening of the channels allows some of the chemical to flow out and exhange with the substantial amount of K+ outside the cell. Once this occurs, the membrane potential of the neuron is switched.

The next part in the system is the propagation of the axon. The process is a two part system dealing with depolarization, which is a positive change across the membrane potential, and repolarization, which is returning a neuron to the resting potential it was first at. Depolarization begins with the opening of voltage-gated Na+ channels along the axon. Once one of these is open, the rest of the channels begin to follow the pattern and begin opening up rapidly for very short bursts of time. The channels open to allow the outflow of Na+ into the axon to continue depolarizing the cell by depleting it of the positive charge within.

Repolarization occurs after the depolarization of the axon is finished. The event begins to return to the axon's resting potential by opening the K+ channels on the outside of the Na+ channels and allowing them to dispurse and switch places. This event however only occurs towards the end of the depolarization process (McKinley 2013). Once the places are switched and the channels have finished exchanging, the hyperpolarization period occurs. This is when the axon is slighty above the negative potential it needs to be at (McKinley 2013). This last step is the final conclusion in putting the action potential propagation back into the RMP or resting membrane potential it ends up at so that the potential is allowed to occur again.

Multiple Sclerosis is an autoimmune disease that causes the neurons of a cell to progressively demylenate themselves or lose the mylenation that helps shield them and to transport action potentials. The oligodendrocytes are the creators of the mylein that aids with the action potential but when these are removed, the abilities associated with motor coordination and sensory information processing is impaired. (McKinley 2013). The disease usually occurs between the ages of 18 and 40 (McKinley 2013).