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

2013 ◽  
Vol 39 (1) ◽  
pp. 142-149 ◽  
Author(s):  
Daniel Martínez ◽  
Lucía García ◽  
José Aguilera ◽  
Arturo Ortega

2021 ◽  
Vol 22 (15) ◽  
pp. 7822
Author(s):  
Anton N. Shuvaev ◽  
Olga S. Belozor ◽  
Oleg I. Mozhei ◽  
Elena D. Khilazheva ◽  
Andrey N. Shuvaev ◽  
...  

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.


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

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 ◽  
...  

2008 ◽  
Vol 33 (7) ◽  
pp. 1277-1285 ◽  
Author(s):  
Rossana C. Zepeda ◽  
Iliana Barrera ◽  
Francisco Castelán ◽  
Abraham Soto-Cid ◽  
Luisa C. Hernández-Kelly ◽  
...  

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