نتایج جستجو برای: oligodendrocytes

تعداد نتایج: 4188  

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 1998
E R Bongarzone S G Howard V Schonmann A T Campagnoni

Expression of the dopamine D3 receptor (D3r) was found in primary mixed glial cultures from newborn brain and in the corpus callosum in vivo during the peak of myelination. Expression of the D3r mRNA, but not D2r mRNA, was detected as early as 5 d in vitro (DIV) by RT-PCR. Immunoblot studies revealed D3r protein was also expressed in the cultures. Double immunofluorescence analysis for the D3r ...

Journal: :The Journal of Cell Biology 1999
H. Ueda J.M. Levine R.H. Miller B.D. Trapp

Retinal ganglion cell axons and axonal electrical activity have been considered essential for migration, proliferation, and survival of oligodendrocyte lineage cells in the optic nerve. To define axonal requirements during oligodendrogenesis, the developmental appearance of oligodendrocyte progenitors and oligodendrocytes were compared between normal and transected optic nerves. In the absence ...

Journal: :Molecular pharmacology 2016
Rogelio O Arellano María Victoria Sánchez-Gómez Elena Alberdi Manuel Canedo-Antelo Juan Carlos Chara Aitor Palomino Alberto Pérez-Samartín Carlos Matute

Myelination requires oligodendrocyte-neuron communication, and both neurotransmitters and contact interactions are essential for this process. Oligodendrocytes are endowed with neurotransmitter receptors whose expression levels and properties may change during myelination. However, only scant information is available about the extent and timing of these changes or how they are regulated by olig...

Journal: :Glia 1998
D M Lang M Monzón-Mayor C E Bandtlow C A Stuermer

Retinal ganglion cell (RGC) axons in lizards (reptiles) were found to regenerate after optic nerve injury. To determine whether regeneration occurs because the visual pathway has growth-supporting glia cells or whether RGC axons regrow despite the presence of neurite growth-inhibitory components, the substrate properties of lizard optic nerve myelin and of oligodendrocytes were analyzed in vitr...

Journal: :The Journal of neuroscience : the official journal of the Society for Neuroscience 2013
Wensheng Lin Yifeng Lin Jin Li Ali G Fenstermaker Sharon W Way Benjamin Clayton Stephanie Jamison Heather P Harding David Ron Brian Popko

There is compelling evidence that oligodendrocyte apoptosis, in response to CNS inflammation, contributes significantly to the development of the demyelinating disorder multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). Therefore, approaches designed to protect oligodendrocytes would likely have therapeutic value. Activation of pancreatic endoplasmic retic...

Journal: :Glia 1996
D M Lang C A Stuermer

Xenopus oligodendrocytes and aspects of their differentiation were analyzed in vitro and in vivo using cell- and stage-specific antibodies. Undifferentiated oligodendrocytes were derived from optic nerves or spinal cords. They divided in vitro, were of elongated shape, were glial fibrillary acidic protein and O4 positive, transiently exhibited several antigens including HNK-1 and L1, and promot...

Journal: :Neuronal Signaling 2021

Journal: :Journal of Cerebral Blood Flow & Metabolism 2003

2010
Iryna Ziabreva Graham Campbell Julia Rist Jessica Zambonin Joanna Rorbach Mateusz M Wydro Hans Lassmann Robin J M Franklin Don Mahad

Oligodendrocyte lineage cells are susceptible to a variety of insults including hypoxia, excitotoxicity, and reactive oxygen species. Demyelination is a well-recognized feature of several CNS disorders including multiple sclerosis, white matter strokes, progressive multifocal leukoencephalopathy, and disorders due to mitochondrial DNA mutations. Although mitochondria have been implicated in the...

Journal: :Annals of neurology 2003
Jennifer L Takahashi Fabrizio Giuliani Christopher Power Yoshinori Imai V Wee Yong

Glutamate excitotoxicity is implicated in the progressive loss of oligodendrocytes in multiple sclerosis, but how glutamate metabolism is dysregulated in the disease remains unclear. Because there is microglia activation in all stages of multiple sclerosis, we determined whether a microglia product, interleukin-1beta, could provide the mechanism for glutamate excitotoxicity. We found that where...

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