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Astrocytes, despite some shared features as glial cells supporting neuronal function in gray and white matter, participate and adapt their morphology and neurochemistry in a plethora of distinct regulatory tasks in specific neural environments. In the white matter, a large proportion of the processes branching from the astrocytes' cell bodies establish contacts with oligodendrocytes and the myelin they form, while the tips of many astrocyte branches closely associate with nodes of Ranvier. Stability of myelin has been shown to greatly depend on astrocyte-to-oligodendrocyte communication, while the integrity of action potentials that regenerate at nodes of Ranvier has been shown to depend on extracellular matrix components heavily contributed by astrocytes. Several lines of evidence are starting to show that in human subjects with affective disorders and in animal models of chronic stress there are significant changes in myelin components, white matter astrocytes and nodes of Ranvier that have direct relevance to connectivity alterations in those disorders. Some of these changes involve the expression of connexins supporting astrocyte-to-oligodendrocyte gap junctions, extracellular matrix components produced by astrocytes around nodes of Ranvier, specific types of astrocyte glutamate transporters, and neurotrophic factors secreted by astrocytes that are involved in the development and plasticity of myelin. Future studies should further examine the mechanisms responsible for those changes in white matter astrocytes, their putative contribution to pathological connectivity in affective disorders, and the possibility of leveraging that knowledge to design new therapies for psychiatric disorders.
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http://dx.doi.org/10.20900/jpbs.20230001 | DOI Listing |
bioRxiv
August 2025
School of Health Sciences, Purdue University, West Lafayette, IN 47907, USA.
Chronic exposure to lead (Pb) is known to cause deficits in neuronal function across the nervous system, including the visual nervous system. Visual deficits have been observed in both humans and rodent models following Pb exposure. However, how Pb exposure causes visual deficits is poorly understood.
View Article and Find Full Text PDFAlzheimers Dement
September 2025
Department of Physiology, College of Basic Medical Sciences, Liaoning Provincial Key Laboratory of Cerebral Diseases, Dalian Medical University, Dalian, China.
Introduction: Alzheimer's disease (AD) neuropathology exhibits early accumulation of amyloid beta (Aβ) plaques within the perforant pathway. This study explores how tenascin-R, a myelin-associated protein at nodes of Ranvier (NORs), modulates Aβ generation through Nav1.6 within this cortico-hippocampal circuit.
View Article and Find Full Text PDFJ Peripher Nerv Syst
September 2025
Department of Neurology, Yonsei University College of Medicine, Seoul, Korea.
Background: Autoimmune nodopathy (AN) is caused by autoantibodies targeting the nodes of Ranvier or paranodes. AN frequently affects cranial nerves and spinal nerve roots and may accompany central demyelination, all of which belong to the intrathecal compartment. We aimed to ascertain the frequency of intrathecal antibody synthesis and blood-CSF barrier (BCSFB) dysfunction in AN and their clinical correlates.
View Article and Find Full Text PDFJ Physiol
August 2025
Visual Neuroscience, Department of Neuroscience, Carl von Ossietzky University Oldenburg, Oldenburg, Germany.
In contrast to most parts of the vertebrate nervous system, ganglion cell axons in the retina typically lack myelination. In the majority of species, ganglion cell axons only become myelinated after leaving the retina to form the optic nerve. The avian retina, however, presents a remarkable exception in that ganglion cell axons are partly myelinated in the retinal nerve fibre layer.
View Article and Find Full Text PDFCells
August 2025
Translational Neurodegeneration Section "Albrecht Kossel", Department of Neurology, University Medical Center Rostock, 18147 Rostock, Germany.
Fatty-acid-hydroxylase-associated neurodegeneration (FAHN) is a rare neurodegenerative disorder caused by loss-of-function mutations in the gene, leading to impaired enzymatic activity and resulting in myelin sheath instability, demyelination, and axonal degeneration. In this study, we established a human in vitro model using neurons and oligodendrocytes derived from induced pluripotent stem cells (hiPSCs) of a FAHN patient. This coculture system enabled the investigation of myelination processes and myelin integrity in a disease-relevant context.
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