The permeability of the tight junctional system of myelin, at the juxtanodal myelin terminal loops and Schmidt-Lanterman incisures, was investigated using the ionic tracer lanthanum (a) in vivo followed by fixation, (b) concurrently with fixation, (c) following fixation. Employing the same methods the juxtanodal membrane complex formed between myelin loops and axolemma was also tested. The results of this study demonstrate that the periaxonal space (between axon and Schwann cell) is apparently accessible to lanthanum via the myelin loop-axolemmal junction, irrespective of the mode of exposure of myelinated fibres to the tracer. Similarly, the tight junctions between adjacent myelin terminal loops apparently do not prevent lanthanum penetration either in living or in fixed nerves. By contrast the tracer obtained access to the extracellular space within incisures only in vivo. The results are interpreted in terms of the permeability of nodes and incisures in vivo to physiologically important ions and related to current concepts of the electrophysiology of the myelinated nerve fibre.
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Anat Sci Int
March 2022
Center for Medical Education, Teikyo University of Science, 2-2-1 Senjusakuragi, Adachi-ku, Tokyo, 120-0045, Japan.
The preparation of histological specimens from animals and humans is a multi-step process comprising tissue collection, fixation, and dehydration, followed by paraffin embedding. Each process can be achieved using different methods and substances. For example, dehydration may not be required depending on the substance used for embedding.
View Article and Find Full Text PDFJ Neurosci
August 2021
Centre for Research in Neuroscience, BRAiN program, Research Institute of the McGill University Health Centre, Montreal, Quebec H3G 1A4, Canada
Iron is an essential cofactor for several metabolic processes, including the generation of ATP in mitochondria, which is required for axonal function and regeneration. However, it is not known how mitochondria in long axons, such as those in sciatic nerves, acquire iron Because of their close proximity to axons, Schwann cells are a likely source of iron for axonal mitochondria in the PNS. Here we demonstrate the critical role of iron in promoting neurite growth using iron chelation.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
November 2020
Section on Molecular Signal Transduction, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892;
Better understanding myelination of peripheral nerves would benefit patients affected by peripheral neuropathies, including Charcot-Marie-Tooth disease. Little is known about the role the Golgi compartment plays in Schwann cell (SC) functions. Here, we studied the role of Golgi in myelination of peripheral nerves in mice through SC-specific genetic inactivation of phosphatidylinositol 4-kinase beta (PI4KB), a Golgi-associated lipid kinase.
View Article and Find Full Text PDFEur J Histochem
March 2020
Department of Anatomy, Histology, Forensic Medicine and Orthopedics, Sapienza University of Rome.
Schwann cells (SC) are characterized by a remarkable plasticity that enables them to promptly respond to nerve injury promoting axonal regeneration. In peripheral nerves after damage SC convert to a repair-promoting phenotype activating a sequence of supportive functions that drive myelin clearance, prevent neuronal death, and help axon growth and guidance. Regeneration of peripheral nerves after damage correlates inversely with thrombin levels.
View Article and Find Full Text PDFJ Neurosci
April 2016
Neuroscience Institute and Departments of Neuroscience and Physiology and Neurology, New York University-Langone Medical Center, New York, New York 10016,
Unlabelled: The signaling pathways that regulate myelination in the PNS remain poorly understood. Phosphatidylinositol-4,5-bisphosphate 3-kinase 1A, activated in Schwann cells by neuregulin and the extracellular matrix, has an essential role in the early events of myelination. Akt/PKB, a key effector of phosphatidylinositol-4,5-bisphosphate 3-kinase 1A, was previously implicated in CNS, but not PNS myelination.
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