Myelin entails a fatty substance which is produced in the central nervous system and insulates axons, thus speeding the rate at which information is transmitted from a cell to another. It is found in the Schwann cell membrane in the central nervous system and is responsible for insulation. The brain of a human being undergoes extensive maturation throughout life to facilitate cognitive development by the use of myelin axon, which is vital in the maturation process. Notably, nerve fibers are long to ensure that impulses are traveling between distant parts of the body (Allen & Barres, 2009). A significant number of different mechanisms have expanded to optimize the propagation of action potential along axon because it needs an active flow of current. Therefore, the existence of myelin in an axon speeds up transmission velocity in different ways.
The myelin of axon speeds up velocity by increasing the transmission of the action potential along a myelinated axon through insulating the axon, thereby, reducing the axonal membrane capacity. The myelin of axon also speeds up velocity by decreasing the ability of neuron in the area it covers in the body. Neurons at negative membrane potential have a considerable number of agitated negative ions that lacks a positive ion to balance them. Myelin wraps around the cell where it gives a layer between the inner and outer part of the cell. The presence of myelin makes the loss of ions across the membrane impossible, thus helping in preserving the action potential (Allen & Barres, 2009). Therefore, it speeds up the velocity by reducing the magnitude of the repulsing force that would prevent the movement of ions in the body.
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The myelin of axon speeds up the velocity of the action potential by insulating the axon. Thus, there is assembling the specialized molecular structure which is done at the lumps of Ranvier. In myelinated nerve fibers, trans-membrane occurs at the lumps of Ranvier where axon membrane is exposed. Since myelin is made up of lipids, it speeds up the velocity of the action potential by acting as an insulator along with the internodal parts. For instance, conduction velocity in a significant number of myelinated axons can influence this velocity.
Besides, myelin speeds up the velocity by increasing the diameter of an axon where current flow is enhanced, thus reducing its internal resistance during transmission. Notably, myelin enables the rapid conduction of action potential by localizing voltage ions and acting as an electrical insulator. Chiefly, the voltage at nodes is highly accumulated, thus being responsible for generating an action potential (Pajevic, Basser & Fields, 2014). There are specific molecules which have nodal axons to induce and maintain nodal clusters. Myelin acts by assembling this nodal molecular organization where the action potential in these nerve fibers shifts from node to another.
Therefore, myelin can significantly enhance the speed of conduction velocity in the neurons since it insulates the axon and arranges the voltage sodium clusters at separate nodes along its length. The damage or failure of myelin can cause excess problems in the body. It causes various neurological diseases, which includes multiple sclerosis among others since transmission of nerve impulses is slowed (Pajevic, Basser & Fields, 2014). At this stage, the impulses have to flow along the entire nerve fiber since it cannot jump from node to node.
Essay Question Two
Neurons communicate by secreting neurotransmitters into a synaptic fissure, which is the gap between the sending neuron and the receiving neuron. After the recognition of a particular neurotransmitter by the post-synaptic receptor, it is then taken back into the synaptic crevice. Here, it must be deactivated faster to prevent it from continually stimulating the post-synaptic cells and unnecessary dismissal of action budding. Neurotransmitters include Serotonin responsible for mood, sleep, appetite, sensory perception, and a role in mental discomforts. Acetylcholine manipulates muscle coordination, cognitive function, eye movements, as well as sleeping. Dopamine impacts on progress, memory, and learning and plays a significant role in both Schizophrenia and Parkinson disease (Eulenburg & Gomeza, 2010). Norepinephrine affects learning and memory. Epinephrine affects emotional arousal and memory storage. GABA, Gama aminobutyric acid, plays a role in neural inhibition in the central nervous system.
Transport proteins remove and deactivate some neurotransmitters from the synaptic cleft. This protein carrier works by carrying the neurotransmitters into the Pre-synaptic cubicle, where it is put in a vesicle or stored until when in required to convey a chemical message. Serotonin is detached and deactivated by transport proteins through re-uptake, a process vulnerable to drug exploitation. The amount of serotonin increases in the synaptic cleft is enhanced by blocking the action of serotonin re-uptake inhibitors. A careful serotonin reuptake inhibitor acts mainly at the 5HT protein carrier (Eulenburg & Gomeza, 2010). The selective serotonin reuptake inhibitor binds to transport protein and blocks the reuptake procedure. As a result, the more serotonin which is left in the synaptic fissure is free to move and retort with the near receptors. Antagonists requisite on serotonin reuptake inhibitors is dependent on extracellular sodium ions; Na+.
There are many selective serotonin reuptake inhibitors in the market and under research for development: those available entail citalopram, fluoxetine, fluvoxamine, paroxetine, and sertraline. Moreover, abusive drugs like cocaine, fenfluramine, and methamphetamine are inhibitors of serotonin uptake. Antidepressant medications also bind on serotonin due to their high resemblance for the transporter and so, inhibiting serotonin from combining and the transporter from tossing inside the pre-synaptic cell. Cocaine, using serotonin inhabitation action, has been extensively used in the diagnosis of Horner's pupil, without determining whether it is postganglionic or preganglionic lesion (Dani, 2010). The main advantage of Protein Transporters is that it protects against overstimulation and allows the localization of the response. The disadvantage is it is relatively slow.
Another mode of deactivating a neurotransmitter is enzyme inactivation of neurotransmitters. Not all neurotransmitters are recycled in the presynaptic cell since others are quickly diffused away from the receptors. Acetylcholine has a specific enzymatic inactivation neurotransmitter known as Acetylcholinesterase. This enzyme is available in all cholinergic synapses, which play a vital role in deactivating Acetylcholine by hydrolysis. Acetylcholinesterase breaks acetylcholine into acetate and choline; its component parts. After hydrolysis, acetate spreads faster into the nearby medium while choline is taken to the presynaptic cubicles through a high-affinity choline uptake system. Anticholinesterases are a class of enzymes that take the place of acetylcholine at an active site and thereby reducing neurotransmitters ability to bind. Releasing acetylcholine into the synaptic cleft binds a postsynaptic receptor and then splits into acetate and choline. Clinically this technique is used in the treatment of Alzheimer's disease and the Myasthenia Gravis. Some of the enzyme inactivation neurotransmitters are its speed in giving the effect (Dani, 2010). It is faster, direct, and specific to a particular neurotransmitter, depending on the enzyme. The disadvantages include the impact of chemicals on this enzyme. Chemicals like poisons, aesthetics, and certain drugs affect these enzymes.
References
Allen, N. J., & Barres, B. A. (2009). Neuroscience: glia—more than just brain glue. Nature , 457 (7230), 675.
Dani, A., Huang, B., Bergan, J., Dulac, C., & Zhuang, X. (2010). Superresolution imaging of chemical synapses in the brain. Neuron , 68 (5), 843-856.
Eulenburg, V., & Gomeza, J. (2010). Neurotransmitter transporters expressed in glial cells as regulators of synapse function. Brain research reviews , 63 (1-2), 103-112.
Pajevic, S., Basser, P. J., & Fields, R. D. (2014). Role of myelin plasticity in oscillations and synchrony of neuronal activity. Neuroscience , 276 , 135-147.
