1.Immunocytochemical localization of myelin basic protein, proteolipid protein and myelin-associated glycoprotein in human oligodendrocyte in culture.
Korean Journal of Anatomy 1991;24(1):86-92
No abstract available.
Humans*
;
Myelin Basic Protein*
;
Myelin Sheath*
;
Myelin-Associated Glycoprotein*
;
Oligodendroglia*
2.Effect of Glutathione on Methylmercury-induced Neurotoxicity in Cultured Bovine Oligodendrocytes.
Seung Taeck PARK ; Jae Min OH ; Min kyo CHOI ; Jung Joong KIM ; Hyang Suk YOON ; Jin Won CHUNG ; Ick Kyu PARK ; Byung Hun LEON ; Won Sin KIM ; Yeun Tai CHUNG
Korean Journal of Physical Anthropology 1997;10(1):47-53
No abstract available.
Glutathione*
;
Oligodendroglia*
3.Interactions Between Astrocytes and Oligodendroglia in Myelin Development and Related Brain Diseases.
Xuelian HU ; Guangdan YU ; Xiang LIAO ; Lan XIAO
Neuroscience Bulletin 2023;39(3):541-552
Astrocytes (ASTs) and oligodendroglial lineage cells (OLGs) are major macroglial cells in the central nervous system. ASTs communicate with each other through connexin (Cx) and Cx-based network structures, both of which allow for quick transport of nutrients and signals. Moreover, ASTs interact with OLGs through connexin (Cx)-mediated networks to modulate various physiological processes in the brain. In this article, following a brief description of the infrastructural basis of the glial networks and exocrine factors by which ASTs and OLGs may crosstalk, we focus on recapitulating how the interactions between these two types of glial cells modulate myelination, and how the AST-OLG interactions are involved in protecting the integrity of the blood-brain barrier (BBB) and regulating synaptogenesis and neural activity. Recent studies further suggest that AST-OLG interactions are associated with myelin-related diseases, such as multiple sclerosis. A better understanding of the regulatory mechanisms underlying AST-OLG interactions may inspire the development of novel therapeutic strategies for related brain diseases.
Humans
;
Myelin Sheath
;
Astrocytes
;
Oligodendroglia
;
Brain
;
Brain Diseases
4.Proteomics as a Tool for Understanding Schizophrenia.
Clinical Psychopharmacology and Neuroscience 2011;9(3):95-101
Schizophrenia is likely to be a multifactorial disorder, consequence of alterations in gene and protein expression since the neurodevelopment that together to environmental factors will trigger the establishment of the disease. In the post-genomic era, proteomics has emerged as a promising strategy for revealing disease and treatment biomarkers as well as a tool for the comprehension of the mechanisms of schizophrenia pathobiology. Here, there is a discussion of the potential pathways and structures that are compromised in schizophrenia according to proteomic findings while studying five distinct brain regions of post-mortem tissue from schizophrenia patients and controls. Proteins involved in energy metabolism, calcium homeostasis, myelinization, and cytoskeleton have been recurrently found to be differentially expressed in schizophrenia brains. These findings may encourage new studies on the understanding of schizophrenia biochemical pathways and even new potential drug targets.
Biomarkers
;
Brain
;
Calcium
;
Comprehension
;
Cytoskeleton
;
Energy Metabolism
;
Homeostasis
;
Humans
;
Myelin Sheath
;
Oligodendroglia
;
Proteins
;
Proteomics
;
Schizophrenia
5.Carbonic anhydrase II immunostaining in the cerebellum of postnatal mice.
Chang Ho YOON ; Gye Sun JEON ; Cheol LEE ; Je Hoon SEO ; Tae Cheon KANG ; Kyeong Han PARK ; Choong Ik CHA ; Sang Ho BAIK ; Sa Sun CHO
Korean Journal of Anatomy 1999;32(4):535-541
The carbonic anhydrase II (CA-II) is specifically expressed in oligodendrocytes, the cells responsible for myelination in the central nervous system. However no direct evidence on relationship between myelin formation and CA-II immunoreactivity has been described. The aims of these studies are to investigate the relationship between CA-II and myelination during cerebellar development of mouse. Myelin staining was found on postnatal (P) 14, and its intensity increased in proportion to developmental age. CA-II positive oligodendrocytes were observed in the white matter of cerebellum on P 14 day. CA-II positive oligoden-drocytes also occured in the granular layer and Purkinje cell layers in the later stage of dvelopment. The parallel development in the CA-II expression and myelination during development suggests that CA-II in oligoendrocyte play a role to myelination.
Animals
;
Carbon*
;
Carbonic Anhydrase II*
;
Carbonic Anhydrases*
;
Central Nervous System
;
Cerebellum*
;
Mice*
;
Myelin Sheath
;
Oligodendroglia
6.Protective effect of transplantation of human oligodendrocyte precursor cells in a rat model of white matter injury.
Xin ZHONG ; Zuo LUAN ; Jing ZANG ; Qian GUAN ; Yin-Xiang YANG ; Qian WANG ; Yuan SHI
Chinese Journal of Contemporary Pediatrics 2021;23(4):410-415
OBJECTIVE:
To study the effect of human oligodendrocyte precursor cell (hOPC) transplantation in the treatment of white matter injury (WMI).
METHODS:
Neonatal rats were randomly divided into a sham-operation group, a model group, and a transplantation group (
RESULTS:
The place navigation test using the Morris water maze showed that the model group had a significantly longer escape latency than the sham-operation group, and compared with the model group, the transplantation group had a significant reduction in escape latency (
CONCLUSIONS
Intrathecal hOPC transplantation may alleviate neurological injury and promote remyelination in a rat model of WMI.
Animals
;
Animals, Newborn
;
Humans
;
Myelin Sheath
;
Oligodendrocyte Precursor Cells
;
Oligodendroglia
;
Rats
;
White Matter
7.Chronic Exposure to Hypoxia Inhibits Myelinogenesis and Causes Motor Coordination Deficits in Adult Mice.
Lin CHEN ; Shu-Yu REN ; Rui-Xue LI ; Kun LIU ; Jing-Fei CHEN ; Yu-Jian YANG ; Yong-Bin DENG ; Han-Zhi WANG ; Lan XIAO ; Feng MEI ; Fei WANG
Neuroscience Bulletin 2021;37(10):1397-1411
Exposure to chronic hypoxia is considered to be a risk factor for deficits in brain function in adults, but the underlying mechanisms remain largely unknown. Since active myelinogenesis persists in the adult central nervous system, here we aimed to investigate the impact of chronic hypoxia on myelination and the related functional consequences in adult mice. Using a transgenic approach to label newly-generated myelin sheaths (NG2-CreER
Animals
;
Clemastine
;
Hypoxia/complications*
;
Mice
;
Mice, Inbred C57BL
;
Mice, Transgenic
;
Myelin Sheath
;
Oligodendroglia
8.The Relationship between Anti-Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease and the Rubella Virus.
Seok Jin CHOI ; Dan A OH ; Woochang CHUN ; Sung Min KIM
Journal of Clinical Neurology 2018;14(4):598-600
No abstract available.
Glycoproteins*
;
Oligodendroglia*
;
Rubella virus*
;
Rubella*
9.Hypoxic-Ischemic Encephalopathy in Premature Infants: Update on Periventricular Leukomalacia.
Korean Journal of Perinatology 2009;20(2):106-113
Premature birth may lead to subsequent impairment of developmental events related to myelination, especially as a sequel to periventricular leukomalacia (PVL). PVL results in injury to cerebral white matter, characterized most commonly (80~90% of cases) by a diffuse abnormality consisting of astrogliosis and injury to premyelinating oligodendrocytes. The major long-term motor complication of the focal component of PVL is spastic diplegia, the major prominent motor deficit subsequently observed in premature infants. Although cerebral white matter disease has been considered the principal result of PVL of the premature infant, more recent findings from quantitative MRI studies suggest that gray matter disease is a common and important accompaniment. Here I will review up-to-date delineation of novel neuropathology/pathogenesis, clinical aspects and neuroprotective trials as well as classification and incidence of PVL.
Cerebral Palsy
;
Humans
;
Hypoxia-Ischemia, Brain
;
Incidence
;
Infant, Newborn
;
Infant, Premature
;
Leukoencephalopathies
;
Leukomalacia, Periventricular
;
Myelin Sheath
;
Oligodendroglia
;
Parturition
10.Effects of Fetal Spinal Cord Transplants on Injured Rat Spinal Cord.
Jee Youn LEE ; Chang Rak CHOI ; Byung Tae AHN
Journal of Korean Neurosurgical Society 2004;35(1):95-101
OBJECTIVE: Previous studies have demonstrated that axon regeneration or remyelination after spinal cord injury occurs when provided with a suitable substratum such as fetal spinal cord (FSC). We carry out this study to determine whether FSC transplants can reduce the glial scar at the interface between host and graft. METHODS: Hemisectioned spinal cord injury was made by aspiration at T3 or T4 spinal cord level in rat. Cell suspension of E-14 FSC was introduced into the injured cavity contaning glial scar tissue. To indentify the transplanted cells from host tissue, FSC cells were labeled with DiI. Rats were sacrificed at 1, 2, 3, and 8 weeks after transplanation and spinal cord was undergone serial sections for immunocytochemistry and histological observation. The observation by electron microscope was carried out too. RESULTS: We could observe that the FSC transplants survived in host spinal cord and generally occupied most of the neuron-depleted area. Examination of serial sections through the graft-host interface which had been immunoreacted for glial fibrillary acidic protein demonstrated that the glial scar was no longer a continuous wall separating the graft and host tissues at eight weeks after injury. We could observe oligodendrocyte and the reformed myelin at the interface by electron microscope. CONCLUSION: The fetal spinal cord transplant can reduce an established glial scar or restrict the reformation of a scar following surgical manipulation, and that the FSC transplant can promote remyelination.
Animals
;
Axons
;
Cicatrix
;
Glial Fibrillary Acidic Protein
;
Immunohistochemistry
;
Myelin Sheath
;
Oligodendroglia
;
Rats*
;
Regeneration
;
Spinal Cord Injuries
;
Spinal Cord*
;
Transplants