Pathophysiology of Multiple Sclerosis - Report

Added on - Jan 2020

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Action potentials along the myelin sheath and node of Ranvier: Pathophysiology ofmultiple sclerosis1Action potentials along the myelin sheath and node of Ranvier: Pathophysiology ofMultiple SclerosisStudent's Name:Instructor's Name:Date:
Action potentials along the myelin sheath and node of Ranvier: Pathophysiology ofmultiple sclerosis2Introduction:The axon in the central nervous system (CNS) is typically a neuronal process of considerablelength [1]. The primary function of this process of neuronal origin is to conduct electricalimpulses or ‘action potentials’ carrying information to the nerve ending/ terminal from the bodyof the cell [1]. In the peripheral and central nervous systems (PNS and CNS respectively), thereare essentially two types of axons present: myelinated and unmyelinated i.e. containing a myelinsheath or not containing it [1]. The myelinated axons are further composed of three segments: i)summation point of somatic inputs in an initial segment where the action potential is generated;ii) a second segment which effectively transmits the action potential in pulses of action potentialchain and it is usually of variable length; iii)The final segment is the preterminal end of the axonleading to the region beyond where the expansion of the synaptic terminal occurs [1]. Theinitiation of the action potential does not occur solely in the first composite segment of the axonbut also occurs in the second segment where the reliable transmission of the action potentialoccurs [1]. There is absence of attenuation in the second segment of the myelinated axon [1, 2].For the correct functioning of the CNS and the PNS, it is crucial that there is an efficient transferof information in the axons in the form of action potentials [2]. Research has indicated thatmyelination is largely responsible for the increase in the speed of axonal conduction [2]. Themyelin sheath present on the axon allows for the rapid transmission of action potential to thenerve terminal from the cell body [2]. The increased speed of axonal conduction ensuresenhanced efficiency of cognitive functionality [2]. Axonal conduction velocity, when accuratelyregulated, leads to an improved coordination of motor neuronal skills and integration of sensoryperceptions and functionality [2]. Most neuropathologies thus conversely reflect the disruption
Action potentials along the myelin sheath and node of Ranvier: Pathophysiology ofmultiple sclerosis3and dysfunction in two primary specialised structures of axons that are vital for rapid axonalconduction: a) the myelin sheath and b) the node of Ranvier [2]. The disruption of these two vitalstructures of the axon leads to alterations in sensory perception, output of motor skills, andcognitive processing [2]. Literature has several instances where the dysfunction of the node ofRanvier is indicated as a crucial factor in the pathogenesis of most neurological disorders [2].Myelin sheath and the node of Ranvier: role in axonal propogation ofaction potentials:In vertebrates, the rapid transmission of electrical impulses occurs across considerably largedistances [2]. Such transmission occurs through myelinated axons via the process of ‘saltatoryconduction’. The speed of conduction is higher in axons which are covered by a myelin sheath[2, 3]. The myelin sheath is produced in the PNS by Schwann cells and oligodendrocytic cells inthe CNS [2, 3]. The myelin sheath is rich in lipids and is a multilayered structure [2]. Theeffective resistance present in the axonal membrane is increased by the myelin sheath byincreasing the length of the electrical space constant and in turn increasing the speed of thesignals across the axon [2, 3]. Consequently, the effective capacitance value of the membrane ofthe axon is increased leading to a minimal amount of charge or sodium influx threshold valuerequired for the depolarization of the cell [2, 3]. These effects resulting from the myelin sheathactivity lead to the total speed of conduction of the action potential in the axons [2].Additionally, there is a marked reduction in the amount of sodium atoms that enter the cellleading to a reduction in the expenditure of ATP that occurs in the axon during sodium pumping[2]. The energy efficiency of the axon and in turn the action potential conduction ability is
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