Murine oligodendroglial cells express nerve growth factor.

Byravan, Sujatha; Foster, Lyndon M.; Phan, Tram; Verity, A. Neil; Campagnoni, Anthony T.

doi:10.1073/pnas.91.19.8812

Cited by 71 publications

(41 citation statements)

References 44 publications

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“…Mice lacking proteolipid protein (PLP) develop a delayed-onset axonopathy with a slow and progressive loss of nerve fibres, consistent with the interpretation that myelinated axons require continual local oligodendrocyte support (Griffiths et al, 1998). Although the precise nature of the oligodendrocyte-derived signal(s) was not determined in these studies, Byravan et al (1994) have demonstrated NGF production by primary oligodendrocyte and OPC cultures, after observations that an oligodendrocyte cell line influences neurite outgrowth in the PC12 adrenal chromaffin cell line. Similarly, oligodendrocyte precursor and immature oligodendrocyte cell lines produce mRNA for members of the glial cell line-derived neurotrophic factor (GDNF) family (Strelau and Unsicker, 1999).…”

Section: Discussionmentioning

confidence: 57%

A role for oligodendrocyte‐derived IGF‐1 in trophic support of cortical neurons

Wilkins¹,

Chandran²,

Compston³

2001

Glia

166

115

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Neurons and glia interact in the development of mammalian central nervous systems and in the maintenance of stable myelinated axons. Recent evidence suggests a role for oligodendrocytes in providing trophic support for neurons during development and in the mature nervous system. This work prompted us to study oligodendrocyte influences on neuronal survival and death in vitro. Rat embryonic cortical neurons were co-cultured with purified oligodendrocytes at different developmental stages and separately with oligodendrocyte-conditioned medium. Neuronal survival was measured by immunocytochemistry and 3H-GABA uptake. Neurons show a marked increase in survival when co-cultured directly with oligodendrocyte precursors (OPCs) and differentiated oligodendrocytes. Neurons cultured in the presence of OPCs separated by a permeable membrane and those cultured in medium conditioned by oligodendrocytes also show a significant increase in survival. Medium conditioned by differentiated oligodendrocytes provides a greater survival effect than medium conditioned by OPCs. Neutralising antibodies to IGF-1, but not to other candidate trophic factors, block the soluble survival effect of oligodendrocytes. Cells of the oligodendrocyte lineage produce IGF-1 and recombinant IGF-1 promotes neuronal survival under identical conditions. This study provides evidence that OPCs and differentiated oligodendrocytes support neuronal survival by both contact-mediated and soluble mechanisms and that IGF-1 significantly contributes to this effect.

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Section: Discussionmentioning

confidence: 57%

A role for oligodendrocyte‐derived IGF‐1 in trophic support of cortical neurons

Wilkins¹,

Chandran²,

Compston³

2001

Glia

166

115

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“…Satellite oligodendrocytes modulate the efficacy of synaptic transmission [36], accumulate extracellular GABA, potassium, chloride and bicarbonate [37][38][39][40]. Additionally, neuronal viability might be compromised due to the loss of oligodendroglial-derived neurotrophins [41]. Thus, depletion of postnatal SVZ cells will likely reduce satellite oligodendrocyte production and, therefore, disturb brain homeostasis.…”

Section: Loss Of Svz Cells Will Reduce Gm Oligodendrogliogenesis Whimentioning

confidence: 99%

Hypoxia/Ischemia Depletes the Rat Perinatal Subventricular Zone of Oligodendrocyte Progenitors and Neural Stem Cells

Levison¹,

Rothstein²,

Romanko³

et al. 2001

Dev Neurosci

162

123

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Cerebral hypoxia/ischemia of the newborn has a frequency of 4/1,000 births and remains a major cause of cerebral palsy, epilepsy, and mental retardation. Despite progress in understanding the pathogenesis of hypoxic-ischemic injury, the data are incomplete regarding the mechanisms leading to permanent brain injury. Here we tested the hypothesis that cerebral hypoxia/ischemia damages stem/progenitor cells in the subventricular zone (SVZ), resulting in a permanent depletion of oligodendrocytes. We used a widely accepted rat model and examined animals at recovery intervals ranging from 4 h to 3 weeks. Within hours after the hypoxic-ischemic insult 20% of the total cells were deleted from the SVZ. The residual damaged cells appeared necrotic. During 48 h of recovery deaths accumulated; however, these later deaths were predominantly apoptotic. Many apoptotic SVZ cells stained with a marker for immature oligodendrocytes. At 3 weeks survival, the SVZ was smaller and markedly less cellular, and it contained less than 1/4 the normal complement of neural stem cells. The corresponding subcortical white matter was dysmyelinated, relatively devoid of oligodendrocytes and enriched in astrocytes. We conclude that neural stem cells and oligodendrocyte progenitors in the SVZ are vulnerable to hypoxia/ischemia. Consequently, the developmental production of oligodendrocytes is compromised and regeneration of damaged white matter oligodendrocytes does not occur resulting in failed regeneration of CNS myelin in periventricular loci. The resulting dysgenesis of the brain that occurs subsequent to perinatal hypoxic/ischemic injury may contribute to the cognitive and motor dysfunction that results from asphyxia of the newborn.

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“…Gray matter oligodendrocytes buffer potassium, chloride and bicarbonate, they accumulate ␥ -amino butyric acid and they produce neurotrophins [Kettenmann et al, 1983;Reynolds and Herschkowitz, 1984;Sapirstein et al, 1984;Levi et al, 1986;Byravan et al, 1994;Dai et al, 2003]. The majority of oligodendrocytes in the gray matter are positioned immediately adjacent to neurons as so-called perineuronal satellite oligodendrocytes.…”

Section: Neocortical Oligodendrocyte Depletion Will Likely Contributementioning

confidence: 99%

Gray Matter Oligodendrocyte Progenitors and Neurons Die Caspase-3 Mediated Deaths Subsequent to Mild Perinatal Hypoxic/Ischemic Insults

Rothstein

Levison²

2005

Dev Neurosci

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With significant improvements in neonatal care, fewer infants sustain severe injury as a consequence of hypoxia/ischemia (H/I). However, the majority of experimental studies have inflicted moderate to severe injuries, or they have assessed damage to the caudal forebrain; therefore, to better understand how a mild H/I episode affects the structures and cells of the rostral forebrain, we assessed the relative vulnerabilities of cells in the neocortex, striatum, corpus callosum, choroid plexus and subventricular zone (SVZ). To inflict mild H/I injury, the right common carotid artery was ligated followed by 1 h of hypoxia (8% O₂) at 37°C. Regional vulnerabilities were assessed using TUNEL, active caspase-3 and hematoxylin and eosin staining at 24 and 48 h of recovery. Scattered columns of cell death were observed in the neocortex with deep-layer neurons more vulnerable than more superficial neurons. The majority of these dying neurons appeared to be dying apoptotic rather than necrotic deaths. In addition, approximately 1/3 of the apoptotic cells in the neocortex were O4+ oligodendrocyte progenitors. We also observed a decrease in NG2 staining within the affected regions of the forebrain. By contrast, active caspase-3+/S-100β+ astrocytes were not observed. Neurons and O4+ oligodendrocyte progenitors also died apoptotic deaths within the striatum. The lining cells of the choroid plexus also sustained damage. Elevated numbers of apoptotic cells were observed in the most lateral region of the SVZ and some of these dying cells were O4+. The most novel finding of this study, that oligodendrocyte progenitors in the gray matter are damaged and eliminated as a consequence of perinatal H/I, provides new insights into the histopathology and neurological deficits observed in infants who sustain mild H/I brain injuries.

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Murine oligodendroglial cells express nerve growth factor.

Cited by 71 publications

References 44 publications

A role for oligodendrocyte‐derived IGF‐1 in trophic support of cortical neurons

A role for oligodendrocyte‐derived IGF‐1 in trophic support of cortical neurons

Hypoxia/Ischemia Depletes the Rat Perinatal Subventricular Zone of Oligodendrocyte Progenitors and Neural Stem Cells

Gray Matter Oligodendrocyte Progenitors and Neurons Die Caspase-3 Mediated Deaths Subsequent to Mild Perinatal Hypoxic/Ischemic Insults

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