post #2: what is actually going down on the neurons

Multiple Sclerosis (MS) is an autoimmune disorder that causes the body’s immune system to attack the central nervous system (CNS). This immune response diminishes the myelin sheaths that surround axons and also damages the nerve fibers underneath the myelin. This attack results in lesions of the axons and eventually results in a lack of insulation for nerve signals. Without these myelin sheaths, the nerve signaling is either slowed or completely blocked. The signals cannot reach the brain quickly or effectively and basic motor function or signaling pathways become greatly compromised. If one were to think of wires that connect to a phone or computer: if the rubber insulating the wire was not there, the charge could disperse to other surrounding objects and make the ending result much weaker or non-existent.


However, this comparison is not completely analogous to multiple sclerosis as the main purpose of the myelin sheaths is not actually to provide insulation for incoming and outgoing nerve signals. Instead the myelin sheaths allow for the neurons to perform saltatory conduction to speed up the slower process of an action potential. In between each myelin sheath is a regulated space of bare neuron that exists only at a length of a few microliters. These spaces between the myelin are called the Nodes of Ranvier (NORs) and are essential to rapid signal transmission. Therefore, the myelin sheaths work in conjunction with the NORs in order to execute saltatory conduction. The word “saltatory” comes from the Latin word “to jump” or “to hop” and describes the process of the sodium and potassium ion charge transferring from one node to the next, thus exponentially increasing the speed of the action potential by decreasing the area through which the charge is conducted.


Action potential is a binary electrical process that occurs in the membrane of our neurons. At what is called resting potential, our neurons are polarized so that they are negatively charged within the membrane and the extracellular space is positively charged. Embedded in the membrane are potassium ion channels and sodium ion channels that open for K+ ions to slowly flow out while Na+ slowly flows in when given a small type of stimulus. This flow of ions causes the depolarization of the membrane and the decrease of the resting concentration gradient, and if the stimulus is significant enough to depolarize the membrane past the threshold, then an action potential will occur. When an action potential occurs, Na+ ions flow rapidly into the membrane while K+ ions flow rapidly out.


Saltatory conduction increases the rate of nerve transmission through action potential from 5 meters/second (11mph) to 150 meters/second (330mph).


The main problem with having this new multitude of unmyelinated nerve fibers (otherwise known as unmedullated) suddenly in the central nervous system lies in the fact that unmyelinated axons are used primarily for sensory nerve signals. These neurons are either unmyelinated or sparsely myelinated, as they travel at much slower speeds and create duller signals. This specific type of nerve structure, the peripheral postganglionic autonomic fibers, has a great deal to do with how our body feels pain. Everyone has stubbed a toe in the past, and the feeling we get at first is a quick shooting pain that then dulls down to a bearable throbbing. Those quick shooting pains are the doing of medullated axons called A delta fibers that send pain signals quickly to the brain, and the slow and dull pulsing pain accounts for the unmedullated fibers named C fibers. Unmyelinated axons are also much smaller and travel shorter distances.


The main goal that researchers are currently working towards is enabling the body to rebuild the diminished myelin and repair the lesions done on the axons and nerve fibers. The primary research being conducted lies in stimulating brain cells and nerve tissue to repair what’s damaged. However, a big issue of MS is that the axons do in fact repair themselves to some extent, but biologists do not understand what prevents full reparations in the CNS.

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