Glia in mammalian development and disease

Zuchero, J. Bradley; Barres, Ben A.

doi:10.1242/dev.129304

Cited by 264 publications

(229 citation statements)

References 52 publications

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“…However, degenerating neurons have been suggested to be capable of inducing astrogliosis, and astrogliosis has been used as an indicating scale for evaluating neuronal damage. [33][34][35][36] The present model of Pb-induced inflammation in the cytoarchitectural profile of the mPFC in juvenile rats exposed to PbNO3 might explain the irreversible neuropathological and neurobehavioral anomalies associated with Pb exposure. [3,37] The functional and structural integrity of the CNS is prone to various forms of insults and toxins that are capable of initiating cascades of deleterious responses.…”

Section: Discussionmentioning

confidence: 99%

Lead induces inflammation and neurodegenerative changes in the rat medial prefrontal cortex

Adekomi¹,

Stephen²,

Adekilekun³

et al. 2017

Anatomy

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Objectives: Lead (Pb) is a neurotoxicant heavy metal ubiquitously present in the eco-system. The precise mechanism by which Pb confers its deleterious effects on the cellular profile of the central nervous system remains unknown. The aim of this study was to investigate the effect of Pb on the medial prefrontal cortex (mPFC) using histological, immunohistological and morphological techniques.Methods: Thirthy juvenile male Wistar rats were used in this study. The rats were randomly assigned into three groups. Group A served as the control group, Group B received 5 mg/kg Pb-nitrate (PbNO3) orally for 21 days, and Group C received 5 mg/kg PbNO3 and left for an additional 21 days to recover.Results: There was a significant decrease in the number of normal neurons in the mPFC of the PbNO3-treated rats. The number of degenerating neurons significantly increased in the PbNO3-treated groups compared with the control group. A marked increase was observed in the number of astrocytic cell count in the PbNO3-treated groups compared with the control. The neuronal cells in the cytoarchitectural profile of the mPFC of the rats receiving PbNO3 showed marked neurodegenerative modification with features of distorted morphology, swollen and vacuolized cytoplasm, and features of either pyknotic or karyorrhectic nuclei. The cytoarchitecture of the mPFC of the rats in the control group preserved the normal histological outline suggestive of a normal and functional mPFC. Conclusion:Exposure to Pb ingestion can result in significant inflammatory responses in the cytoarchitectural profile of the mPFC. Furthermore, 21 days of cessation of exposure to PbNO3 did not halt or reverse the deleterious effects of Pb on the mPFC of the rats, suggesting that Pb persists in the central nervous system of the rats.

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Section: Discussionmentioning

confidence: 99%

Lead induces inflammation and neurodegenerative changes in the rat medial prefrontal cortex

Adekomi¹,

Stephen²,

Adekilekun³

et al. 2017

Anatomy

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“…42 Glia cell abnormalities during development are present. 43 Thank to the inductive activity of the cephalic NCC, that migrated in the subsequent pre-cordal skull base, the superimposed neural tube is transformed into the prosencephalon, which afterwards differentiates into telencephalon and diencephalon. 44 From telencephalon, subcortical GABA-expressing neurons migrate along the radial glia into the neocortex stimulated by Dlx mesencephalon gene activity.…”

Section: Discussionmentioning

confidence: 99%

“…41 Oligodendrocytes precursor cells and oligodendrocytes express the CNS glial transcription factor Sox 10 41,43 which, with Pax 3, promotes in PNS Schwann cell production. 43 All glial cells of the PNS originate directly from NCC. 43 NCC development is regulated by NCC transcription factors.…”

Section: Discussionmentioning

confidence: 99%

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Kearns-Sayre syndrome with facial and white matter extensive involvement: a (mitochondrial and nuclear gene related?) neurocristopathy?

2017

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The Authors report on a patient with Kearns-Sayre syndrome, large mtDNA deletion (7/kb), facial abnormalities and severe central nervous system (CNS) white matter radiological features, commonly attributed to spongy alterations. The common origin from neural crest cell (NCC) of facial structures (cartilagineous, osseous, vascular and of the peripheral nervous system) and of peripheral glia and partially of the CNS white matter are underlined and the facial and glial abnormalities are attributed to the abnormal reproduction/migration of NCC. In this view, the CNS spongy alterations in KSS may be not only a dystrophic process (leukodystrophy) but also a dysplastic condition (leukodysplasia). The Authors hypothesize that the symptoms may be related to mtDNA mutations associated to NCC nuclear gene abnormality.

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“…In addition to the physiological roles, glial cell are deeply involved in pathological conditions such as neurodegenerative and demyelinating disorders in the CNS [2]. The main pathology of these diseases is called neuroinflammation, which is characterized by glial activation along with production of cytokines, radicals and their related substances.…”

Section: Dysfunction Of Glial Cells In Neurological and Psychologicalmentioning

confidence: 99%

Dysfunction of Glial Cells in Neurological and Psychological Disorders: From Bench to Bedside

Katafuchi¹,

Нода²

2016

NIB

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Glia in mammalian development and disease

Cited by 264 publications

References 52 publications

Lead induces inflammation and neurodegenerative changes in the rat medial prefrontal cortex

Lead induces inflammation and neurodegenerative changes in the rat medial prefrontal cortex

Kearns-Sayre syndrome with facial and white matter extensive involvement: a (mitochondrial and nuclear gene related?) neurocristopathy?

Dysfunction of Glial Cells in Neurological and Psychological Disorders: From Bench to Bedside

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