Abstract
Raman, NMR and EPR spectroscopy and electrophysiology methods were used to investigate the excitability and the packaging of myelin lipid layers and its viscosity during nerve exposure to pronase E. It was established that during exposure of nerve to pronase E the action potential (AP) conduction velocity and the Schwann cell (SC) (or myelin) water ordering increases, but the nerve myelin refractive index and internode incisions numbers decrease. This effect included two periods–short- and long-time period, probably, because the first one depends on SC protein changes and the second one–on the nerve fiber internode demyelination. It was concluded that high electrical resistance of myelin, which is important for a series of AP conduction velocity, not only depends on nerve fiber diameter and the myelin lipid composition, but also on the regularity of myelin lipid fatty acids and myelin lipid layer packing during the axoglial interaction.
Highlights
Repetitive excitation of a nerve fiber is known to result in accumulation of extracellular K+, especially between the axon and the myelin [1,2]
We have studied the effects of the proteolytic enzyme pronase E on the nerve excitation (AP amplitude and action potential (AP) conduction velocity)
That during nerve exposure to pronase the node of Ranvier (NR) length increases and the numbers of the incisions decrease (Fig 3). This changes both increase myelin lipid layer packing and its electrical resistance and the number of NR channels, which leads to an increase in the AP conduction velocity
Summary
Repetitive excitation of a nerve fiber is known to result in accumulation of extracellular K+, especially between the axon and the myelin [1,2]. Uptake of K+ leads to Schwann cell (SC) swelling and myelin restructuring that impacts its electrical properties In some pathology, such as nerve ischemia, demyelination, and disruptions of junctions between the axon and glial cell (CNS), which fails to cope with the K+ uptake, fluxing out through the open K+-channels of the internode axolemma. Because of this failure, K+ accumulates in the confined extracellular space between the axon and the sheath (internode space), and to a lesser extent around the node of Ranvier (NR) and outside of the fiber. Analysis of K+ -currents in rat nerve fibers after demyelination during the perfusion with pronase or lysolecitin suggests the existence of two fast and one slow potassium channels populations, similar in the nodal membrane of frog nerve fibers [3,4]
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