Modulation of oligodendrocyte generation during a critical temporal window after NG2 cell division

Hill, Robert A.; Patel, Kiran D.; Gonçalves, Christopher M.; Grutzendler, Jaime; Nishiyama, Akiko

doi:10.1038/nn.3815

Cited by 164 publications

(197 citation statements)

References 54 publications

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“…But after whisker removal, the density of oligodendrocytes was smaller in the deprived somatosensory cortex (i.e., barrel cortex region). 64 Also, subventricular zone-derived OPCs receive synaptic input in the white matter in a mouse model of remyelination, suggesting that similar to a developmental myelination, remyelination may be partially mediated by neuronal activity. 65 By contrast, some axonal surface ligands suppress oligodendrocyte differentiation/maturation.…”

Section: Oligodendrocyte-neuron Interactionmentioning

confidence: 99%

Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury

Shindo

Liang

Maki

et al. 2015

J Cereb Blood Flow Metab

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Oligodendrocytes are one of the major cell types in cerebral white matter. Under normal conditions, they form myelin sheaths that encircle axons to support fast nerve conduction. Under conditions of cerebral ischemia, oligodendrocytes tend to die, resulting in white-matter dysfunction. Repair of white matter involves the ability of oligodendrocyte precursors to proliferate and mature. However, replacement of lost oligodendrocytes may not be the only mechanism for white-matter recovery. Emerging data now suggest that coordinated signaling between neural, glial, and vascular cells in the entire neurovascular unit may be required. In this mini-review, we discuss how oligodendrocyte lineage cells participate in signaling and crosstalk with other cell types to underlie function and recovery in various experimental models of subcortical white-matter injury.

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Section: Oligodendrocyte-neuron Interactionmentioning

confidence: 99%

Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury

Shindo

Liang

Maki

et al. 2015

J Cereb Blood Flow Metab

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“…Considering that most peripheral tissues contain less than 1 mM L2-HG and are quite normal in L2hgdh KO mice, intracellular L-2-HG levels may need to reach a higher level (i.e., Ͼ1 mM) to cause pathological changes. Postnatal week 2 is crucial for CNS pathology in L2hgdh KO mice, as it is a critical time point for OPC differentiation, oligodendrocyte maturation, and axon myelination in the mouse brain (42,43). Myeli-…”

Section: Fig 5 Legend (Continued)mentioning

confidence: 99%

L2hgdh Deficiency Accumulates l-2-Hydroxyglutarate with Progressive Leukoencephalopathy and Neurodegeneration

Ma¹,

Sun²,

Jiang³

et al. 2017

Molecular and Cellular Biology

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L-2-Hydroxyglutarate aciduria (L-2-HGA) is an autosomal recessive neurometabolic disorder caused by a mutation in the L-2-hydroxyglutarate dehydrogenase (L2HGDH) gene. In this study, we generated L2hgdh knockout (KO) mice and observed a robust increase of L-2-hydroxyglutarate (L-2-HG) levels in multiple tissues. The highest levels of L-2-HG were observed in the brain and testis, with a corresponding increase in histone methylation in these tissues. L2hgdh KO mice exhibit white matter abnormalities, extensive gliosis, microglia-mediated neuroinflammation, and an expansion of oligodendrocyte progenitor cells (OPCs). Moreover, L2hgdh deficiency leads to impaired adult hippocampal neurogenesis and late-onset neurodegeneration in mouse brains. Our data provide in vivo evidence that L2hgdh mutation leads to L-2-HG accumulation, leukoencephalopathy, and neurodegeneration in mice, thereby offering new insights into the pathophysiology of L-2-HGA in humans.KEYWORDS L2HGDH, 2-HG, leukoencephalopathy, gliosis, neurodegeneration T he rare, autosomal recessive neurometabolic disorders D-2-hydroxyglutaric aciduria (D-2-HGA) and L-2-hydroxyglutaric aciduria (L-2-HGA) are characterized by the accumulation of D-2-hydroxyglutarate (D-2-HG) and L-2-hydroxyglutarate (L-2-HG), respectively, in body fluids. Genetic characterization has shown that 50% of the D-2-HGA population and the majority of L-2-HGA patients harbor pathogenic mutations in D2HGDH and L2HGDH genes, respectively (1-3). The other half of D-2-HGA patients have a gain-of-function mutation in isocitrate dehydrogenase 2 (IDH2) at the residue of R140 (R140Q), which leads to abnormally high accumulation of D-2-HG (4). Based on phenotypic severity in patients, D-2-HGA is classified as mild type I (D2HGDH mutation) and severe type II (IDH2 mutation) (4, 5). Of note, 2-HG concentrations are 2-to 8-fold higher for type II D-2-HGA than type I D-2-HGA patients (4, 6, 7), suggesting that

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“…For instance, deprivation of sensory experiences by removing whiskers at critical periods in early postnatal development was shown to drastically increase OPC proliferation and alter OPC distribution, as well as lead to decreased innervation of OPCs by M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT thalamocoritcal neurons (Mangin et al 2012). Through the use of in vivo imaging of the somatosensory cortex after whisker removal, Hill and colleagues demonstrated a slight increase in OPC proliferation coupled with a reduction in oligodendrocyte production (Hill et al 2014). Although, precise results from the various investigations differed, the studies all pointed to the labile nature of oligodendrocyte lineage cells during sensory experiences, particularly during critical periods.…”

Section: Neural Activitymentioning

confidence: 99%

Behavioral experiences as drivers of oligodendrocyte lineage dynamics and myelin plasticity

2016

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Many behavioral experiences are known to promote hippocampal neurogenesis. In contrast, the ability of behavioral experiences to influence the production of oligodendrocytes and myelin sheath formation remains relatively unknown. However, several recent studies indicate that voluntary exercise and environmental enrichment can positively influence both oligodendrogenesis and myelination, and that, in contrast, social isolation can negatively influence myelination. In this review we summarize studies addressing the influence of behavioral experiences on oligodendrocyte lineage cells and myelin, and highlight potential mechanisms including experience-dependent neuronal activity, metabolites, and stress effectors, as well as both local and systemic secreted factors. Although more study is required to better understand the underlying mechanisms by which behavioral experiences regulate oligodendrocyte lineage cells, this exciting and newly emerging field has already revealed that oligodendrocytes and their progenitors are highly responsive to behavioral experiences and suggest the existence of a complex network of reciprocal interactions among oligodendrocyte lineage development, behavioral experiences, and brain function. Achieving a better understanding of these relationships may have profound implications for human health, and in particular, for our understanding of changes in brain function that occur in response to experiences. This article is part of the Special Issue entitled 'Oligodendrocytes in Health and Disease'.

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Modulation of oligodendrocyte generation during a critical temporal window after NG2 cell division

Cited by 164 publications

References 54 publications

Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury

Subcortical ischemic vascular disease: Roles of oligodendrocyte function in experimental models of subcortical white-matter injury

L2hgdh Deficiency Accumulates l-2-Hydroxyglutarate with Progressive Leukoencephalopathy and Neurodegeneration

Behavioral experiences as drivers of oligodendrocyte lineage dynamics and myelin plasticity

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