Regulation of Glial Function by Insulin Peptides
André Kleinridders in Physiological Consequences of Brain Insulin Action, 2023
Oligodendrocytes were also first described by del Rio-Hortega (81), and are the myelinating cells of the CNS, while Schwann cells are their counter-part in the peripheral nervous system. Both are from neuroepithelial lineage. Oligodendrocyte precursors (usually refer as NG-2 glia) remain in high numbers in the adult brain and constitute a renewal pool for these glial cells, generated all along ontogeny. Accordingly, this source of precursor cells is important for endogenous re-myelination (82) and is modulated by ILPs (83, 84). Myelinated axons are a key component of the mammalian brain, providing fast conductance capacities to neurons and forming the white matter of the brain. Other roles of oligodendroglia in the adult CNS that are increasingly emerging (85), may also be regulated by ILPs, but more work is needed.
Propagation of the Action Potential
Nassir H. Sabah in Neuromuscular Fundamentals, 2020
The solution, in the form of myelinated axons, is ingeniously simple and highly effective. The axon is surrounded by a myelin sheath consisting of up to 200 layers or so of passive cell membrane interrupted at regular intervals in what are referred to as the nodes of Ranvier (Figure 4.7). The region between adjacent nodes is the internode, whose length is roughly 100–150 times the axon diameter and ranges in length between about 200 µm and 2.5 mm, depending on axon diameter. The sheath is wrapped around the axon during embryonic development by specialized satellite cells of the nervous system – the glial cells (Section 1.2.3). In the central nervous system, the glial cells that form the myelin sheath are referred to as oligodendrocytes, with each oligodendrocyte forming one internode of myelin for up to about 50 adjacent axons. In the peripheral nervous system, a glial cell referred to as a Schwann cell forms one internode of only a single axon.
Vitamin C in Neurological Function and Neurodegenerative Disease
Qi Chen, Margreet C.M. Vissers in Vitamin C, 2020
Oligodendrocytes can repair and restore damaged myelin, but not at the speed with which the myelin is destroyed by demyelinating lesions. It has been suggested that increasing the population of oligodendrocytes could attenuate the axonal degeneration caused by chronic lesions [271]. Cerebral injection of fetal glial progenitor cells increased myelination in several regions of the brain and rescued the phenotype in congenitally hypomyelinated shiverer mice [272]. Both mature and premyelinating oligodendrocytes have been visualized in lesions collected from patient autopsy; however, there was little evidence of effective remyelination, presumably due to the disruption in the microenvironment necessary to maintain the relationship between oligodendrocytes and axons [273]. It is long established that vitamin C is necessary for Schwann cell myelination in the peripheral nervous system due to its role in collagen synthesis [274], but vitamin C also appears to play a crucial role in the differentiation of oligodendrocyte progenitor cells into mature oligodendrocytes [275].
The role of microRNA in neuronal inflammation and survival in the post ischemic brain: a review
Published in Neurological Research, 2023
William A. Li, Aslan Efendizade, Yuchuan Ding
Cerebral ischemia induces neurogenesis and angiogenesis in adult human and rodent models, which have been studied in depth compared to stroke-induced oligodendrogenesis. Oligodendrocytes (OL), myelin-forming cells in the central nervous system, are vulnerable to cerebral ischemia. Loss of oligodendrocytes and their myelin impairs axonal function and is detrimental to functional recovery. As expected, the therapies that aim to prevent myelin loss or promote myelin regeneration are critical to neuronal survival and subsequent functional and cognitive recovery after ischemia. Serum response factor (SRF) plays a crucial role in the maturation of OL, and when SRF is inhibited, differentiation of oligodendrocyte progenitor cells is arrested [64,65]. Buller et al. demonstrated that ischemic stroke causes an up-regulation of SRF and down-regulation of miR-9 and miR-200b in OL white matter [64]. The same study also found that miR-9 and miR-200 target the SRF 3′-UTR directly and down-regulate the translation of SRF mRNA [64]. This indicates that miR-9 and miR-200b play an important role in stroke-induced SRF up-regulation in oligodendrocyte progenitor cells and mature oligodendrocytes, which ultimately affects oligodendrocyte progenitor cell differentiation. Most recent study has shown miR-9 is down-regulated in mice with MCAO brain and oxygen–glucose deprivation neurons. Elevation of miR-9 restored the neurological scores and reduced the infarct volume, brain water content and behavioral impairments [66].
Nanoparticles-based anti-aging treatment of Alzheimer’s disease
Published in Drug Delivery, 2022
Jian-Jian Chu, Wen-Bo Ji, Jian-Hua Zhuang, Bao-Feng Gong, Xiao-Han Chen, Wen-Bin Cheng, Wen-Danqi Liang, Gen-Ru Li, Jie Gao, You Yin
In the CNS, myelin is an extension of oligodendrocytes concentrically wrapped around nerve axons (Kuhn et al., 2019). Functionally, myelin facilitates rapid transmission of axonal potentials and provides metabolic support to wrapped nerve axons. They are highly vulnerable to oxidative stress (Giacci et al., 2018). White matter changes in AD are thought to reflect both demyelination and axonal damage (Prins & Scheltens, 2015), while SA-β-Gal upregulation of oligodendrocyte in human cerebral tissue of white matter lesion (WML) may be evidence of oligodendrocyte senescence in AD (Al-Mashhadi et al., 2015). In the brains of human patients with AD and APP/PS1 mice model, OPCs with high expression of senescent phenotypes (p21, p16, and SA-β-Gal) were correlated with amyloid plaques, whereas in age-matched subjects without dementia, these senescent phenotypes were not obvious (Zhang et al., 2019). OPCs are very important for myelin regeneration following injury (Kuhn et al., 2019). Young mice had highly active myelination, while in aged mice, it was greatly inhibited, which coincides with spatial memory deficits (Wang et al., 2020). The impaired function of senescent OPCs may play a crucial role in disease progression, and reduced self-healing capacity could be due to the aging process and pathological factors such as Aβ deposition or NFT (Cai & Xiao, 2016; Zhang et al., 2019).
The promotive effect of activation of the Akt/mTOR/p70S6K signaling pathway in oligodendrocytes on nerve myelin regeneration in rats with spinal cord injury
Published in British Journal of Neurosurgery, 2020
Chen Ge, Dong Liu, Yongming Sun
Oligodendrocytes are a type of glial cell involved in producing myelin sheaths in the central nervous system (CNS).5 Oligodendrocytes are especially susceptible to the toxicity of the acute lesion environment that occurs after SCI.6 They undergo both acute apoptosis and necrosis, with apoptosis persisting chronically. The Akt/mTOR signaling pathway is known to be involved in oligodendrocyte development through controlling oligodendrocyte precursor cell (OPC) proliferation, survival, differentiation, migration, and myelination. It is known that the Akt pathway has promotive effects on oligodendrocyte differentiation and myelination. For instance, inappropriate cleavage of neuregulin decreases the phosphorylation of Akt in mice,7 and IGF-1 promotes the maintenance of Akt phosphorylation in oligodendroglia,8 which also has an important role in CNS myelination in vivo. Furthermore, the mTOR pathway plays an active role in the differentiation of oligodendrocytes, but not in astrocytes or neurons.9