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cx43 white matter

Melissa L Cooper, John W Collyer, David J Calkins
Astroyctes serve myriad functions but are especially critical in white matter tracts, where energy-demanding axons propagate action potentials great distances between neurons. Axonal dependence on astrocytes for even normal function accentuates the critical role astrocytes serve during disease. In glaucoma, the most common optic neuropathy, sensitivity to intraocular pressure (IOP) challenges RGC axons early, including degradation of anterograde transport to the superior colliculus (SC). Astrocyte remodeling presages overt axon degeneration in glaucoma and thus may present a therapeutic opportunity...
May 10, 2018: Acta Neuropathologica Communications
Qiong Wang, Zhen Wang, Yeye Tian, Huaqiu Zhang, Yongkang Fang, Zhiyuan Yu, Wei Wang, Minjie Xie, Fengfei Ding
Oligodendrocyte precursor cells (OPCs) proliferation and differentiation are essential for remyelination after white matter injury. Astrocytes could promote oligodendrogenesis after white matter damage whereas the underlying mechanisms are unknown. In this study, the role of astrocytic connexin43 (Cx43) hemichannels involved in OPC proliferation and differentiation in chronic hypoxia was evaluated. In an astrocyte-OPC co-culture chronic hypoxia model, OPCs became proliferative but failed to mature into oligodendrocytes...
April 2018: Journal of Molecular Neuroscience: MN
Serge Nataf, Marc Barritault, Laurent Pays
We previously reported that, in multiple sclerosis (MS) patients with a progressive form of the disease, spinal cord periplaques extend distance away from plaque borders and are characterized by the co-occurrence of partial demyelination, astrocytosis and low-grade inflammation. However, transcriptomic analyses did not allow providing a comprehensive view of molecular events in astrocytes vs. oligodendrocytes. Here, we re-assessed our transcriptomic data and performed co-expression analyses to characterize astrocyte vs...
October 5, 2017: International Journal of Molecular Sciences
G G Kovacs, A Yousef, S Kaindl, V M Lee, J Q Trojanowski
AIMS: Ageing-related tau astrogliopathy (ARTAG) appears in subependymal, subpial, perivascular, white matter (WM) and grey matter (GM) locations. Physical effects, blood-brain barrier dysfunction and blood- or vessel-related factors have been considered as aetiology. As connexin-43 (Cx43) and aquaporin-4 (AQP4) are related to these, we hypothesized that their immunoreactivity (IR) varies with ARTAG in a location-specific manner. METHODS: We performed a morphometric immunohistochemical study measuring the densities of IR of Cx43, AQP4, AT8 (phospho-tau) and glial fibrillar acidic protein (GFAP)...
July 29, 2017: Neuropathology and Applied Neurobiology
Panos Theofilas, Christian Steinhäuser, Martin Theis, Amin Derouiche
Connexin 43 (Cx43) is the main astrocytic connexin and forms the basis of the glial syncytium. The morphology of connexin-expressing cells can be best studied in transgenic mouse lines expressing cytoplasmic fluorescent reporters, since immunolabeling the plaques can obscure the shapes of the individual cells. The Cx43kiECFP mouse generated by Degen et al. (FASEBJ 26:4576, 2012) expresses cytosolic ECFP and has previously been used to establish that Cx43 may not be expressed by all astrocytes within a population, and this can vary in a region-dependent way...
March 30, 2017: Journal of Neuroscience Research
Karina Goncharenko, Eftekhar Eftekharpour, Alexander A Velumian, Peter L Carlen, Michael G Fehlings
Gap junctions are widely present in spinal cord white matter; however, their role in modulating the dynamics of axonal dysfunction remains largely unexplored. We hypothesized that inhibition of gap junctions reduces the loss of axonal function during oxygen and glucose deprivation (OGD). The functional role of gap junctions was assessed by electrophysiological recordings of compound action potentials (CAPs) in Wistar rat spinal cord slices with the sucrose gap technique. The in vitro slices were subjected to 30-min OGD...
November 1, 2014: Journal of Neurophysiology
Oliver Tress, Marta Maglione, Dennis May, Tatjyana Pivneva, Nadine Richter, Julia Seyfarth, Sonja Binder, Armin Zlomuzica, Gerald Seifert, Martin Theis, Ekrem Dere, Helmut Kettenmann, Klaus Willecke
In this study, we have investigated the contribution of oligodendrocytic connexin47 (Cx47) and astrocytic Cx30 to panglial gap junctional networks as well as myelin maintenance and function by deletion of both connexin coding DNAs in mice. Biocytin injections revealed complete disruption of oligodendrocyte-to-astrocyte coupling in the white matter of 10- to 15-d-old Cx30/Cx47 double-deficient mice, while oligodendrocyte-to-oligodendrocyte coupling was maintained. There were no quantitative differences regarding cellular networks in acute brain slices obtained from Cx30/Cx47 double-null mice and control littermates, probably caused by the upregulation of oligodendrocytic Cx32 in Cx30/Cx47 double-deficient mice...
May 30, 2012: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Kyriaki Markoullis, Irene Sargiannidou, Natasa Schiza, Andreas Hadjisavvas, Federico Roncaroli, Richard Reynolds, Kleopas A Kleopa
Oligodendrocyte gap junctions (GJs) are vital for central nervous system myelination, but their involvement in multiple sclerosis (MS) pathology remains unknown. The aim of this study was to examine alterations of oligodendrocyte and related astrocyte GJs in MS lesions and normal-appearing white matter (NAWM). Post-mortem brain samples from 9 MS and 11 age-matched non-MS control patients were studied. Tissue sections that included both chronic active and inactive lesions were characterized neuropathologically with Luxol Fast Blue staining and immunostaining for myelin oligodendrocyte glycoprotein (MOG) and the microglial marker Iba1...
June 2012: Acta Neuropathologica
Kyriaki Markoullis, Irene Sargiannidou, Christopher Gardner, Andreas Hadjisavvas, Richard Reynolds, Kleopas A Kleopa
Gap junctions (GJs) are vital for oligodendrocyte survival and myelination. In order to examine how different stages of inflammatory demyelination affect oligodendrocyte GJs, we studied the expression of oligodendrocytic connexin32 (Cx32) and Cx47 and astrocytic Cx43 in the experimental autoimmune encephalomyelitis (EAE) mouse model of multiple sclerosis (MS) induced by recombinant myelin oligodendrocyte glycoprotein. EAE was characterized by remissions and relapses with demyelination and axonal loss. Formation of GJ plaques was quantified in relation to the lesions and in normal appearing white matter (NAWM)...
July 2012: Glia
Sarah E Lutz, Cedric S Raine, Celia F Brosnan
We showed previously that mice deficient in astrocyte gap junctions Cx43 and Cx30 exhibit white matter vacuolation and hypomyelination. In this study we tested the hypothesis that loss of astrocytic gap junction proteins leads to exacerbation of the primary demyelinating diseases, using experimental autoimmune encephalomyelitis (EAE) as a model system. To test for this, Cx43 floxed mice were crossed with GFAP:Cre, Cx30 null mice to generate mice lacking astrocytic expression of both Cx43 and Cx30 (dKO). EAE was induced using myelin oligodendrocyte glycoprotein (MOG(35-55)) peptide, and mice were monitored for acute expression of disease...
April 2012: Journal of Neuroimmunology
Wei Wu, Weizhong Gu, Xuefeng Xu, Shiqiang Shang, Zhengyan Zhao
OBJECTIVES: To investigate the possible target genes of methyl-CpG-binding protein 2 (MeCP2) that contribute to Rett syndrome (RTT). METHODS: Brain tissues were taken from Mecp2(308/Y) mice or control mice and then subjected to real-time quantitative reverse transcriptase polymerase chain reaction (RT-PCR), immunohistochemical staining, and Western blot analysis for connexin (Cx)43, Cx45, Cx40, Cx32, 2,3-cyclic nucleotide 3-phosphohydrolase (CNPase), and glial fibrillary acidic protein (GFAP)...
March 2012: Neurological Research
Laura M Magnotti, Daniel A Goodenough, David L Paul
CNS glia exhibit a variety of gap junctional interactions: between neighboring astrocytes, between neighboring oligodendrocytes, between astrocytes and oligodendrocytes, and as 'reflexive' structures between layers of myelin in oligodendrocytes. Together, these junctions are thought to form a network facilitating absorption and removal of extracellular K(+) released during neuronal activity. In mice, loss of the two major oligodendrocyte connexins causes severe demyelination and early mortality, while loss of the two major astrocyte connexins causes mild dysmyelination and sensorimotor impairment, suggesting that reflexive and/or oligo-oligo coupling may be more important for the maintenance of myelin than other forms...
July 2011: Glia
Marta Maglione, Oliver Tress, Brigitte Haas, Khalad Karram, Jacqueline Trotter, Klaus Willecke, Helmut Kettenmann
According to previously published ultrastructural studies, oligodendrocytes in white matter exhibit gap junctions with astrocytes, but not among each other, while in vitro oligodendrocytes form functional gap junctions. We have studied functional coupling among oligodendrocytes in acute slices of postnatal mouse corpus callosum. By whole-cell patch clamp we dialyzed oligodendrocytes with biocytin, a gap junction-permeable tracer. On average 61 cells were positive for biocytin detected by labeling with streptavidin-Cy3...
July 2010: Glia
M J Alao, D Bonneau, M Holder-Espinasse, C Goizet, S Manouvrier-Hanu, A Mezel, F Petit, D Subtil, C Magdelaine, D Lacombe
Oculo-dento-digital dysplasia (ODDD) is an autosomal dominant disorder with complete penetrance and high intra- and interfamilial phenotypic variability. The key features in this syndrome are microphthalmia, enamel hypoplasia and syndactyly of the 4th-5th fingers. ODDD is caused by mutations in the connexin 43 gene (GJA1). We report here four patients from three families with GJA1 mutations, one of them diagnosed prenatally. The three mutations (c.52T > C/p.Ser18Pro, c.689_690delTA/p.Tyr230CysfsX6, c.442C > G/p...
January 2010: European Journal of Medical Genetics
Sarah E Lutz, Yongmei Zhao, Maria Gulinello, Sunhee C Lee, Cedric S Raine, Celia F Brosnan
Astrocytes are coupled via gap junctions (GJs) comprising connexin 43 (Cx43) (Gja1) and Cx30 (Gjb6), which facilitate intercellular exchange of ions. Astrocyte connexins also form heterotypic GJs with oligodendrocytic somata and lamellae. Loss of oligodendrocyte gap junctions results in oligodendrocyte and myelin pathology. However, whether loss of astrocyte GJs affects oligodendrocytes and myelin is not known. To address this question, mice with astrocyte-targeted deletion of Cx43 and global loss of Cx30 [double knock-out (dKO)] were studied using Western blotting, immunohistochemistry, electron microscopy, and functional assays...
June 17, 2009: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
W A Roscoe, E Messersmith, A Meyer-Franke, B Wipke, S J Karlik
Alterations in the expression of gap junction proteins have previously been observed in several diseases affecting the central nervous system; however, the status of connexin 43 (Cx43) has not yet been reported in spinal cord remyelination. We studied Cx43 expression in demyelination and remyelination by using a chronic guinea pig model of experimental allergic encephalomyelitis (EAE). Hartley guinea pigs were immunized with homogenized whole CNS and complete Freund's adjuvant. Animals became chronically ill by day 40 postimmunization, and animals with paralysis were entered into the study...
April 2007: Journal of Neuroscience Research
Albert Lai, Dung-Nghi Le, William A Paznekas, Wes D Gifford, Ethylin Wang Jabs, Andrew C Charles
Oculodentodigital dysplasia (ODDD) is a rare developmental disorder characterized by craniofacial and limb abnormalities. Over 35 separate mutations in human connexin43 (Cx43) causing ODDD have been identified. Several mutations are also associated with central nervous system involvement, including white-matter changes detected by magnetic resonance imaging. As Cx43 is abundantly expressed in astrocytes, we hypothesized that the mutant Cx43 proteins that produce neurological dysfunction have abnormal functional characteristics in astrocytes...
February 1, 2006: Journal of Cell Science
N Rochefort, N Quenech'du, P Ezan, C Giaume, C Milleret
In cat visual cortex, neurons acquire progressively mature functional properties during the first postnatal months. The aim of this study was to analyze the development of astrocytes during this period. The patterns of expression of the glial fibrillary acidic protein (GFAP) as well as of two gap junction proteins expressed in astrocytes, connexin43 (Cx43) and connexin30 (Cx30), were investigated by immunohistochemistry and optical density measurements, in visual cortical areas 17 and 18 at four different ages: 2 weeks (postnatal days 12 to 15, P12-15), 1 month (P27-31), 2 months (P60-62) and beyond 1 year...
December 7, 2005: Brain Research. Developmental Brain Research
Elimor Brand-Schieber, Peter Werner, Dumitru A Iacobas, Sanda Iacobas, Michelle Beelitz, Stuart L Lowery, David C Spray, Eliana Scemes
Both multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE), its animal model, involve inflammatory attack on central nervous system (CNS) white matter, leading to demyelination and axonal damage. Changes in astrocytic morphology and function are also prominent features of MS and EAE. Resting astrocytes form a network that is interconnected through gap junctions, composed mainly of connexin43 (Cx43) protein. Although astrocytic gap junctional connectivity is known to be altered in many CNS pathologies, little is known about Cx43 expression in inflammatory demyelinating disease...
June 15, 2005: Journal of Neuroscience Research
N Rochefort, N Quenech'du, L Watroba, M Mallat, C Giaume, C Milleret
In the adult cat, axons running through the corpus callosum interconnect the border between the visual cortical areas 17 and 18 (A17 and A18) of both hemispheres. This specific pattern emerges during postnatal development, under normal viewing conditions (NR), from the elimination of initially exuberant callosal projections. In contrast, if the postnatal visual experience is monocular from birth (MD), juvenile callosal projections are stabilised throughout A17 and A18. The present study aimed at using such a model in vivo to find indications of a contribution of glial cells in the shaping of projections in the developing CNS through interactions with neurones, both in normal and pathological conditions...
April 2002: Journal of Physiology, Paris
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