Preferential Loading of Bergmann Glia with Synthetic Acetoxymethyl Calcium Dyes

2011 ◽  
Vol 2011 (10) ◽  
pp. pdb.prot065813-pdb.prot065813 ◽  
Author(s):  
T. M. Hoogland ◽  
B. Kuhn ◽  
S. S.- H. Wang
Keyword(s):  
Bergmann Glia ◽  
Calcium Dyes

scholarly journals ERBB3-mediated regulation of Bergmann glia proliferation in cerebellar lamination

Development ◽  
2015 ◽  
Vol 142 (3) ◽  
pp. 522-532 ◽  
Author(s):  
A. Sathyamurthy ◽  
D.-M. Yin ◽  
A. Barik ◽  
C. Shen ◽  
J. C. Bean ◽  
...  
Keyword(s):  
Bergmann Glia

scholarly journals The Molecular Pathway Regulating Bergmann Glia and Folia Generation in the Cerebellum

2017 ◽  
Vol 17 (1) ◽  
pp. 42-48 ◽  
Author(s):  
Alan W. Leung ◽  
James Y. H. Li
Keyword(s):  
Bergmann Glia ◽  
Molecular Pathway

An Acute Glutamate Exposure Induces Long-Term Down Regulation of GLAST/EAAT1 Uptake Activity in Cultured Bergmann Glia Cells

2013 ◽  
Vol 39 (1) ◽  
pp. 142-149 ◽  
Author(s):  
Daniel Martínez ◽  
Lucía García ◽  
José Aguilera ◽  
Arturo Ortega
Keyword(s):  
Bergmann Glia ◽  
Down Regulation ◽  
Glia Cells ◽  
Uptake Activity

scholarly journals Protective Effect of Memantine on Bergmann Glia and Purkinje Cells Morphology in Optogenetic Model of Neurodegeneration in Mice

2021 ◽  
Vol 22 (15) ◽  
pp. 7822
Author(s):  
Anton N. Shuvaev ◽  
Olga S. Belozor ◽  
Oleg I. Mozhei ◽  
Elena D. Khilazheva ◽  
Andrey N. Shuvaev ◽  
...  
Keyword(s):  
Excitatory Amino Acid ◽  
Average Length ◽  
Glutamate Transporter ◽  
Bergmann Glia ◽  
Spinocerebellar Ataxias ◽  
Excitatory Amino Acid Transporter ◽  
Glial Glutamate Transporter ◽  
Gfap Immunoreactivity ◽  
Cerebellar Ataxias ◽  
Receptor Blockers

Spinocerebellar ataxias are a family of fatal inherited diseases affecting the brain. Although specific mutated proteins are different, they may have a common pathogenetic mechanism, such as insufficient glutamate clearance. This function fails in reactive glia, leading to excitotoxicity and overactivation of NMDA receptors. Therefore, NMDA receptor blockers could be considered for the management of excitotoxicity. One such drug, memantine, currently used for the treatment of Alzheimer’s disease, could potentially be used for the treatment of other forms of neurodegeneration, for example, spinocerebellar ataxias (SCA). We previously demonstrated close parallels between optogenetically induced cerebellar degeneration and SCA1. Here we induced reactive transformation of cerebellar Bergmann glia (BG) using this novel optogenetic approach and tested whether memantine could counteract changes in BG and Purkinje cell (PC) morphology and expression of the main glial glutamate transporter—excitatory amino acid transporter 1 (EAAT1). Reactive BG induced by chronic optogenetic stimulation presented increased GFAP immunoreactivity, increased thickness and decreased length of its processes. Oral memantine (~90 mg/kg/day for 4 days) prevented thickening of the processes (1.57 to 1.81 vs. 1.62 μm) and strongly antagonized light-induced reduction in their average length (186.0 to 150.8 vs. 171.9 μm). Memantine also prevented the loss of the key glial glutamate transporter EAAT1 on BG. Finally, memantine reduced the loss of PC (4.2 ± 0.2 to 3.2 ± 0.2 vs. 4.1 ± 0.3 cells per 100 μm of the PC layer). These results identify memantine as potential neuroprotective therapeutics for cerebellar ataxias.

Glutamate transporter GLAST is essential for cytodifferentiation of Bergmann glia and maintenance of excitatory synaptic wiring in the cerebellum

2011 ◽  
Vol 71 ◽  
pp. e63
Author(s):  
Taisuke Miyazaki ◽  
Miwako Yamasaki ◽  
Kouichi Hashimoto ◽  
Keiko Shimamoto ◽  
Kazuhisa Kohda ◽  
...  
Keyword(s):  
Glutamate Transporter ◽  
Bergmann Glia

Glutamate-Dependent Translational Control in Cultured Bergmann Glia Cells: eIF2α Phosphorylation

2013 ◽  
Vol 38 (7) ◽  
pp. 1324-1332 ◽  
Author(s):  
Marco A. Flores-Méndez ◽  
Zila Martínez-Lozada ◽  
Hugo C. Monroy ◽  
Luisa C. Hernández-Kelly ◽  
Iliana Barrera ◽  
...  
Keyword(s):  
Translational Control ◽  
Bergmann Glia ◽  
Glia Cells ◽  
Eif2α Phosphorylation
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