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Electrophysiology of Optic Nerves in Methylglyoxal Treated Mice

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Electrophysiology of Optic Nerves in Methylglyoxal Treated Mice ELECTROPHYSIOLOGY OF OPTIC NERVES IN METHYLGLYOXAL TREATED MICE A thesis submitted in partial fulfillment of the requirements for the degree of Master of Science By PARKER ANDREW VAUGHAN B.S., Wright State University, 2018 2020 Wright State University WRIGHT STATE UNIVERSITY GRADUATE SCHOOL April 24, 2020 I HEREBY RECOMMEND THAT THE THESIS PREPARED UNDER MY SUPERVISION BY Parker Andrew Vaughan ENTITLED Electrophysiology of Optic Nerves in Methylglyoxal Treated Mice BE ACCEPTED IN PARTIAL FULFILLMENT OF THE REQUIREMENTS FOR THE DEGREE OF Master of Science. David R. Ladle, Ph.D. Thesis Director Eric S. Bennett, Ph.D Department Chair Department of Neuroscience, Cell Biology and Physiology Committee on Final Examination David R. Ladle, Ph.D. Patrick M. Sonner, Ph.D. Keiichiro Susuki, MD, Ph.D. Barry Milligan, Ph.D. Interim Dean of the Graduate School ABSTRACT Vaughan, Parker Andrew. M.S. Department of Neuroscience, Cell Biology and Physiology, Wright State University, 2020. Elecrophysiology of Optic Nerves in Methylglyoxal Treated Mice. The nervous system is responsible for interpreting information and coordinating that organism’s physiological response. Action potentials conduct along neuron axons to carry information within the nervous system. Saltatory conduction allows the action potential to travel rapidly along the axon from one Node of Ranvier to the next. Nodes of Ranvier are densely packed with different proteins, notably voltage-gated sodium channels (Nav). Methylglyoxal, a toxic metabolite of glycolysis that is elevated in diabetes mellitus, alters nerve excitability by eliciting changes in protein function and structure within the Nodes of Ranvier. This study investigated the effects of methylglyoxal exposure on nerve conduction in optic nerves of mice, to test the hypothesis that methylglyoxal exposure would decrease conduction velocity. The conduction velocity, peak amplitude, and latency of optic nerve compound action potentials were recorded from saline- and methylglyoxal-treated mice. While results did not reach statistical significance, trends were evident in the analyzed parameters. iii Table of Contents Page I. Introduction……………………………………………………………………1 Action Potential………………………………………………...…………2 Paranode……………………………………………………………….......3 Juxtaparanode…………………………………………………………..…4 Nodes of Ranvier…………………………………………………….……4 Myelin Disease……………………………………………………….……5 Diabetes……………………………………………………………...…….6 Diabetes and Methylglyoxal………………………………………..……..7 Methylglyoxal and Pain………………………………………….………..9 II. Materials and Methods……………………………………………………….13 Animals…………………………………………………………………..13 Dissection Procedures………………………………………...………….13 Extracellular recording of optic nerve action potentials…………………14 Statistical Analyses………………………………………………………14 III. Results………………………………………………………………………..15 Effect of temperature on peak amplitude and conduction velocity……...16 Effects of stimulation intensity on CAP peak amplitude………………...17 Effects of methylglyoxal treatment on optic nerve compound action potential properties……………………………………………………….18 IV. Discussion……………………………………………………………………29 V. References……………………………………………………………………33 iv LIST OF FIGURES Figure Page 1. Optic nerve electrophysiology recorded using suction electrodes…………….…20 2. Extracellular recording of compound action potential in optic nerve……….…...21 3. Peak amplitude increases at physiological temperatures…………………….…..22 4. Conduction velocity increases with increasing temperature……………….…….23 5. Amplitude dramatically increases with increasing stimulus strength until a plateau is reached…………………………………………………..……..24 6. Recording sequence does not correlate with conduction velocity measurements in single optic nerves……………………………………………..25 7. Average peak amplitude does not increase in MG treated mice…………………26 8. Latency values do not increase in MG treated mice……………………………..27 9. Conduction velocity unaffected by methylglyoxal in mouse models…………....28 v I. Introduction The nervous system is responsible for interpreting information and stimuli received from all parts of the body and then coordinating the organism’s physiological response. Information processing takes place primarily in the central nervous system, made up of the brain and spinal cord, and information must travel from the body to these centers to interpret the environment and then back to the peripheral tissues to respond to stimuli. If we are to be efficient and effective organisms, the transmission of information from one part of the body to another must be rapid. One mechanism to increase the conduction velocity of action potential signals along an axon is to surround the axon with an insulating layer of myelin. This is the case for peripheral nerves and major axon pathways in the central nervous system which are myelinated and transmit information across long distances. Myelination enables a rapid mode of action potential transmission called saltatory conduction. Glial cells produce the lipid-rich myelin that insulates axons. Along with providing insulation, the multilayered myelin also decreases membrane capacitance and increases membrane resistance (Hartline, 2008). In myelinated axons, the myelin is arranged along the entirety of the axon in a manner that leaves small spaces of exposed axon between adjacent myelin sheaths. The spaces of exposed nerve fiber interspersed between the myelin sheaths are called Nodes of Ranvier. The nerves that adapt this organization of myelin and internodes can utilize saltatory conduction. Saltatory conduction allows the action potential to travel along the axon, bypassing the areas of the axon that are myelinated and “jump” from one Node of Ranvier to the next. Nodes of Ranvier are densely packed with different proteins, notably voltage-gated sodium channels (Nav). 1 Action Potential The action potential is first generated at the axonal initial segment, or the AIS, and is then propagated along the axon to its destination, bypassing the regions of the axon that are insulated by the myelin sheathing. If the membrane of the nerve has been depolarized enough to reach the threshold, then an action potential will propagate down the length of an axon in a waveform. The polarization of the neuron is dependent upon the concentration gradients across the membrane of the cell. The inside of the cell has a negative charge in relation to the outside of the cell, resulting in a resting potential of around -75 mV. This net negative value is due to the movement of potassium out of the cell, relative to the movement of sodium into the cell. This difference in concentration of ions across the cell membrane is what drives each ion towards its own equilibrium. When a neuron cell membrane reaches threshold, it is the drive of sodium and potassium towards their respective concentration equilibriums that results in the depolarization and subsequent repolarization of the cell membrane. Once the threshold is reached and the depolarization is great enough, there will be an increase in sodium influx into the cell relative to the outward flow of potassium ions. Due to positive feedback, the charge of the inside of the cell will continue to become further depolarized as it drives to reach its sodium equilibrium at +55mV. As the cell nears equilibrium and the sodium channels are fully opened, the influx of sodium ions will slow and the sodium channel pores will begin to close. During this time, the permeability of the potassium will increase the flow of potassium ions out of the cell will increase. This change will, in turn, drive the cell towards the equilibrium voltage of potassium, resulting in rapid repolarization of the cell membrane. As the voltage of the cell reaches its normal resting membrane potential, the 2 potassium channels begin to close. However, the potassium channels close slowly, resulting in an after-hyperpolarization of the membrane as the membrane potential briefly drops below the resting membrane potential before returning to -75mV. Given the importance of the structure and function of the Nodes of Ranvier to the efficient and rapid transmission of actional potentials along the axon, the modification of these nodes would likely result in a variety of neurological dysfunctions. The different interactions and modifications of various proteins found in and around the nodes of Ranvier result in different neurological diseases and dysfunctions. The Nodes of Ranvier can be divided into several different regions, each containing a variety of different proteins that characterize each domain. A Node of Ranvier is flanked on each side with a portion of the myelin sheath called the paranode. Immediately adjacent to the paranode is a region referred to as the juxtaparanode. Paranode The paranode, the region of the myelin on either side of the nodes of Ranvier, is a region of tightly packed myelin that forms glial loops that are filled with cytoplasm. The paranodal region of the axon is characterized by two protein complexes, contactin- associated protein (Caspr) and contactin. Both contactin and Caspr are transmembrane proteins that are involved in cell-to-cell adhesion and communication. (Poliak & Peles, 2003). The importance of Caspr and contactin to the intercellular adhesion is evidenced by the fact that the absence of such protein complexes will result in an increased distance between the axon and the paranodal loops (Poliak & Peles, 2003). Juxtaparanode 3 The juxtaparanode is a small region of the myelin sheath that is immediately adjacent to the paranode, opposite of the Node of Ranvier. The
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