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Bergmann glia

Toru Takahashi, Kazuhiro Nakaso, Yosuke Horikoshi, Takehiko Hanaki, Miho Yamakawa, Masato Nakasone, Yoshinori Kitagawa, Taisuke Koike, Tatsuya Matsura
BACKGROUND: Vitamin E (VE, α-tocopherol) is a fat-soluble vitamin and is well known as an antioxidant. A deficiency in VE induces oxidative stress in the brain and causes motor and memory dysfunction. The consumption of a VE-rich diet has been given much attention in recent years, in regards to anti-aging and the prevention of age-related neuronal disorders. METHODS: A VE-deficient mouse model was prepared by feeding the animals a diet lacking VE. In addition, to evaluate the effect of VE-containing rice bran (RB) on VE deficiency, a diet including RB was also provided...
September 2016: Yonago Acta Medica
Hannah Klein, Glenda K Rabe, Bahri Karacay, Daniel J Bonthius
Lymphocytic choriomeningitis virus (LCMV) infection during pregnancy injures the human fetal brain. Neonatal rats inoculated with LCMV are an excellent model of congenital LCMV infection because they develop cerebellar injuries similar to those in humans. To evaluate the role of T-lymphocytes in LCMV-induced cerebellar pathology, congenitally athymic rats, deficient in T-lymphocytes were compared with euthymic rats. Peak viral titers and cellular targets of infection were similar, but viral clearance from astrocytes was impaired in the athymic rats...
September 25, 2016: Journal of Neuropathology and Experimental Neurology
Q-Z Zhang
Dystroglycanopathies are muscular dystrophies caused by mutations in genes involved the in O-linked glycosylation of α-dystroglycan. Severe forms of these conditions result in abnormalities in exhibit brain and ocular developmental too, in addition to muscular dystrophy. The full spectrum of developmental pathology is caused mainly by loss of dystroglycan from Bergmann glia. Moreover, cognitive deficits are constant features of severe forms of dystroglycanopathies. However, the precise molecular mechanism leading to neuronal dysfunction in these diseases is not fully known yet...
September 2016: European Review for Medical and Pharmacological Sciences
Paola Caporali, Francesco Bruno, Giampiero Palladino, Jessica Dragotto, Laura Petrosini, Franco Mangia, Robert P Erickson, Sonia Canterini, Maria Teresa Fiorenza
Niemann-Pick type C1 (NPC1) disease is a lysosomal storage disorder caused by defective intracellular trafficking of exogenous cholesterol. Purkinje cell (PC) degeneration is the main sign of cerebellar dysfunction in both NPC1 patients and animal models. It has been recently shown that a significant decrease in Sonic hedgehog (Shh) expression reduces the proliferative potential of granule neuron precursors in the developing cerebellum of Npc1 (-/-) mice. Pursuing the hypothesis that this developmental defect translates into functional impairments, we have assayed Npc1-deficient pups belonging to the milder mutant mouse strain Npc1 (nmf164) for sensorimotor development from postnatal day (PN) 3 to PN21...
2016: Acta Neuropathologica Communications
Emma M Perkins, Daumante Suminaite, Yvonne L Clarkson, Sin Kwan Lee, Alastair R Lyndon, Jeffrey D Rothstein, David Ja Wyllie, Kohichi Tanaka, Mandy Jackson
Clinical phenotypes of spinocerebellar ataxia type-5 (SCA5) and spectrin-associated autosomal recessive cerebellar ataxia type-1 (SPARCA1) are mirrored in mice lacking β-III spectrin (β-III(-/-)). One function of β-III spectrin is the stabilisation of the Purkinje cell-specific glutamate transporter EAAT4 at the plasma membrane. In β-III(-/-) mice EAAT4 levels are reduced from an early age. In contrast levels of the predominant cerebellar glutamate transporter GLAST, expressed in Bergmann glia, only fall progressively from 3 months onwards...
August 15, 2016: Human Molecular Genetics
Ruben G F Hendriksen, Sandra Schipper, Govert Hoogland, Olaf E M G Schijns, Jim T A Dings, Marlien W Aalbers, Johan S H Vles
OBJECTIVE: Dystrophin is part of a protein complex that connects the cytoskeleton to the extracellular matrix. In addition to its role in muscle tissue, it functions as an anchoring protein within the central nervous system such as in hippocampus and cerebellum. Its presence in the latter regions is illustrated by the cognitive problems seen in Duchenne Muscular Dystrophy (DMD). Since epilepsy is also supposed to constitute a comorbidity of DMD, it is hypothesized that dystrophin plays a role in neuronal excitability...
2016: Frontiers in Cellular Neuroscience
Yusuke Sawada, Ayumu Konno, Jun Nagaoka, Hirokazu Hirai
Neuron-specific enolase (NSE) is a glycolytic isoenzyme found in mature neurons and cells of neuronal origin. Injecting adeno-associated virus serotype 9 (AAV9) vectors carrying the NSE promoter into the cerebellar cortex is likely to cause the specific transduction of neuronal cells, such as Purkinje cells (PCs) and interneurons, but not Bergmann glia (BG). However, we found BG-predominant transduction without PC transduction along a traumatic needle tract for viral injection. The enhancement of neuroinflammation by the co-application of lipopolysaccharide (LPS) with AAV9 significantly expanded the BG-predominant area concurrently with the potentiated microglial activation...
2016: Scientific Reports
Orquidia G Mendez-Flores, Luisa C Hernández-Kelly, Edna Suárez-Pozos, Mustapha Najimi, Arturo Ortega
Glutamate, the main excitatory neurotransmitter in the vertebrate brain, exerts its actions through specific membrane receptors present in neurons and glial cells. Over-stimulation of glutamate receptors results in neuronal death, phenomena known as excitotoxicity. A family of sodium-dependent, glutamate uptake transporters mainly expressed in glial cells, removes the amino acid from the synaptic cleft preventing neuronal death. The sustained sodium influx associated to glutamate removal in glial cells, activates the sodium/potassium ATPase restoring the ionic balance, additionally, glutamate entrance activates glutamine synthetase, both events are energy demanding, therefore glia cells increase their ATP expenditure favouring glucose uptake, and triggering several signal transduction pathways linked to proper neuronal glutamate availability, via the glutamate/glutamine shuttle...
September 2016: Neurochemistry International
Teresa García-Lezana, Marc Oria, Jordi Romero-Giménez, Jordi Bové, Miquel Vila, Joan Genescà, Laia Chavarria, Juan Cordoba
Hepatic encephalopathy has traditionally been considered a reversible disorder. However, recent studies suggested that repeated episodes of hepatic encephalopathy cause persistent impairment leading to neuronal loss. The aims of our study were the development of a new animal model that reproduces the course of episodic hepatic encephalopathy and the identification of neurodegeneration evidences. Rats with portacaval anastomosis underwent simulated episodes of hepatic encephalopathy, triggered by the regular administration of ammonium acetate, and/or lipopolysaccharide...
May 6, 2016: Journal of Cerebral Blood Flow and Metabolism
Teresa Partearroyo, Juliana Pérez-Miguelsanz, Ángel Peña-Melián, Carmen Maestro-de-Las-Casas, Natalia Úbeda, Gregorio Varela-Moreiras
The brain is particularly sensitive to folate metabolic disturbances, because methyl groups are critical for brain functions. This study aimed to investigate the effects of different dietary levels of folic acid (FA) on postnatal cerebellar morphology, including the architecture and organisation of the various layers. A total of forty male OFA rats (a Sprague-Dawley strain), 5 weeks old, were classified into the following four dietary groups: FA deficient (0 mg/kg FA); FA supplemented (8 mg/kg FA); FA supra-supplemented (40 mg/kg FA); and control (2 mg/kg FA) (all n 10 per group)...
June 2016: British Journal of Nutrition
Ramona Rudolph, Hannah M Jahn, Raphael Courjaret, Nanette Messemer, Frank Kirchhoff, Joachim W Deitmer
Synaptic transmission has been shown to be modulated by glial functions, but the modes of specific glial action may vary in different neural circuits. We have tested the hypothesis, if Bergmann GLIA (BG) are involved in shaping neuronal communication in the mouse cerebellar cortex, using acutely isolated cerebellar slices of wild-type (WT) and of glia-specific receptor knockout mice. Activation of P2Y1 receptors by ADP (100 µM) or glutamatergic receptors by AMPA (0.3 µM) resulted in a robust, reversible and repeatable rise of evoked inhibitory input in Purkinje cells by 80% and 150%, respectively...
July 2016: Glia
Carmen Rubio-Osornio, Aldo Eguiluz-Meléndez, Cristina Trejo-Solís, Veronica Custodio, Moises Rubio-Osornio, Artemio Rosiles-Abonce, Juan C Martínez-Lazcano, Edith González, Carlos Paz
The single feature of all malformations in cortical development is the clinical association with epilepsy. It has been proven that Sox-1 expression is essential during neurodevelopment and it is reported that Sox-1 knockout mice present spontaneous generalized seizures. Particularly in cerebellum, Sox-1 plays a key role in the Bergmann´s glia (BG) function, which allows the correct function of the Purkinje cells (PC). The targets of PC are the dentate and interpositus nuclei, which form the main cerebellar efferents involved in the physiopathology of epilepsy...
2016: CNS & Neurological Disorders Drug Targets
Stephanie Dooves, Marianna Bugiani, Nienke L Postma, Emiel Polder, Niels Land, Stephen T Horan, Anne-Lieke F van Deijk, Aleid van de Kreeke, Gerbren Jacobs, Caroline Vuong, Jan Klooster, Maarten Kamermans, Joke Wortel, Maarten Loos, Lisanne E Wisse, Gert C Scheper, Truus E M Abbink, Vivi M Heine, Marjo S van der Knaap
Vanishing white matter (VWM) is a fatal leukodystrophy that is caused by mutations in genes encoding subunits of eukaryotic translation initiation factor 2B (eIF2B). Disease onset and severity are codetermined by genotype. White matter astrocytes and oligodendrocytes are almost exclusively affected; however, the mechanisms of VWM development remain unclear. Here, we used VWM mouse models, patients' tissue, and cell cultures to investigate whether astrocytes or oligodendrocytes are the primary affected cell type...
April 1, 2016: Journal of Clinical Investigation
Chiara Di Pietro, Daniela Marazziti, Gina La Sala, Zeinab Abbaszadeh, Elisabetta Golini, Rafaele Matteoni, Glauco P Tocchini-Valentini
Cellular primary cilia crucially sense and transduce extracellular physicochemical stimuli. Cilium-mediated developmental signaling is tissue and cell type specific. Primary cilia are required for cerebellar differentiation and sonic hedgehog (Shh)-dependent proliferation of neuronal granule precursors. The mammalian G-protein-coupled receptor 37-like 1 is specifically expressed in cerebellar Bergmann glia astrocytes and participates in regulating postnatal cerebellar granule neuron proliferation/differentiation and Bergmann glia and Purkinje neuron maturation...
March 2, 2016: Cellular and Molecular Neurobiology
Jian-Wei Zhu, Yi-Fei Li, Zhao-Tao Wang, Wei-Qiang Jia, Ru-Xiang Xu
The cerebellum plays an essential role in balance and motor coordination. Purkinje cells (PCs) are the sole output neurons of the cerebellar cortex and are critical for the execution of its functions, including motor coordination. Toll-like receptor (TLR) 4 is involved in the innate immune response and is abundantly expressed in the central nervous system; however, little is known about its role in cerebellum-related motor functions. To address this question, we evaluated motor behavior in TLR4 deficient mice...
2016: Frontiers in Neuroscience
James Cairns, Doug Swanson, Joanna Yeung, Anna Sinova, Ronny Chan, Praneetha Potluri, Price Dickson, Guy Mittleman, Dan Goldowitz
Autism spectrum disorders (ASDs) are a group of neurodevelopmental disorders characterized by impaired and disordered language, decreased social interactions, stereotyped and repetitive behaviors, and impaired fine and gross motor skills. It has been well established that cerebellar abnormalities are one of the most common structural changes seen in the brains of people diagnosed with autism. Common cerebellar pathology observed in autistic individuals includes variable loss of cerebellar Purkinje cells (PCs) and increased numbers of reactive neuroglia in the cerebellum and cortical brain regions...
February 2, 2016: Cerebellum
Adrian Andrzej Chrobak, Zbigniew Soltys
Bergmann glia (BG), a specific type of radial astrocytes in the cerebellum, play a variety of vital functions in the development of this structure. However, the possible role of BG in the development of abnormalities observed in individuals with autism spectrum disorder (ASD) seems to be underestimated. One of the most consistent findings observed in ASD patients is loss of Purkinje cells (PCs). Such a defect may be caused by dysregulation of glutamate homeostasis, which is maintained mainly by BG. Moreover, these glial cells are involved in long-term depression (LTD), a form of plasticity which can additionally subserve neuroprotective functions...
January 26, 2016: Molecular Neurobiology
Natsumi Ageta-Ishihara, Maya Yamazaki, Kohtarou Konno, Hisako Nakayama, Manabu Abe, Kenji Hashimoto, Tomoki Nishioka, Kozo Kaibuchi, Satoko Hattori, Tsuyoshi Miyakawa, Kohichi Tanaka, Fathul Huda, Hirokazu Hirai, Kouichi Hashimoto, Masahiko Watanabe, Kenji Sakimura, Makoto Kinoshita
The small GTPase-effector proteins CDC42EP1-5/BORG1-5 interact reciprocally with CDC42 or the septin cytoskeleton. Here we show that, in the cerebellum, CDC42EP4 is exclusively expressed in Bergmann glia and localizes beneath specific membrane domains enwrapping dendritic spines of Purkinje cells. CDC42EP4 forms complexes with septin hetero-oligomers, which interact with a subset of glutamate transporter GLAST/EAAT1. In Cdc42ep4(-/-) mice, GLAST is dissociated from septins and is delocalized away from the parallel fibre-Purkinje cell synapses...
2015: Nature Communications
Carine Savarin, Cornelia C Bergmann, Melanie Gaignage, Stephen A Stohlman
BACKGROUND: Microbial infections have been implicated in initiating and enhancing severity of autoimmune diseases including the demyelinating disease multiple sclerosis (MS). Nevertheless, the incidence of both acute and persisting viral infections without evidence of autoimmune sequelae suggests that this process is well controlled. The conditions promoting or stemming self-reactive (SR) T cells following viral-induced tissue damage thus need to be better defined. Using a non-fatal viral mouse model of encephalomyelitis associated with demyelination and disability, yet ultimate clinical improvement, this study set out to monitor uptake and presentation of endogenous myelin antigens, as well as induction and fate of SR T cells...
2015: Journal of Neuroinflammation
Jerry Vriend, Saeid Ghavami, Hassan Marzban
Cerebellar granule cells precursors are derived from the upper rhombic lip and migrate tangentially independent of glia along the subpial stream pathway to form the external germinal zone. Postnatally, granule cells migrate from the external germinal zone radially through the Purkinje cell layer, guided by Bergmann glia fibers, to the internal granular cell layer.Medulloblastomas (MBs) are the most common malignant childhood brain tumor. Many of these tumors develop from precursor cells of the embryonic rhombic lips...
2015: Molecular Brain
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