scholarly journals Asymmetric morphogenesis of the parapineal organ in the embryonic zebrafish brain

2017 ◽  
Vol 145 ◽  
pp. S56
Author(s):  
Carmen Gloria Lemus ◽  
Karina Palma ◽  
Jorge Jara ◽  
Teresa Cramer ◽  
Steffen Härtel ◽  
...  
2007 ◽  
Vol 306 (1) ◽  
pp. 302
Author(s):  
Carmen G. Lemus ◽  
Steffen Hartel ◽  
Jenny Regan ◽  
Claire Russel ◽  
Stephen Wilson ◽  
...  

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 637
Author(s):  
Nicholas S. Moore ◽  
Robert A. Mans ◽  
Mackenzee K. McCauley ◽  
Colton S. Allgood ◽  
Keri A. Barksdale

Evidence from human and animal studies indicate that disrupted light cycles leads to alterations of the sleep state, poor cognition, and the risk of developing neuroinflammatory and generalized health disorders. Zebrafish exhibit a diurnal circadian rhythm and are an increasingly popular model in studies of neurophysiology and neuropathophysiology. Here, we investigate the effect of alterations in light cycle on the adult zebrafish brain: we measured the effect of altered, unpredictable light exposure in adult zebrafish telencephalon, homologous to mammalian hippocampus, and the optic tectum, a significant visual processing center with extensive telencephalon connections. The expression of heat shock protein-70 (HSP70), an important cell stress mediator, was significantly decreased in optic tectum of adult zebrafish brain following four days of altered light exposure. Further, pSer473-Akt (protein kinase B) was significantly reduced in telencephalon following light cycle alteration, and pSer9-GSK3β (glycogen synthase kinase-3β) was significantly reduced in both the telencephalon and optic tectum of light-altered fish. Animals exposed to five minutes of environmental enrichment showed significant increase in pSer473Akt, which was significantly attenuated by four days of altered light exposure. These data show for the first time that unpredictable light exposure alters HSP70 expression and dysregulates Akt-GSK3β signaling in the adult zebrafish brain.


2009 ◽  
Vol 5 (4S_Part_6) ◽  
pp. P176-P176
Author(s):  
Alexandra V. Abramsson ◽  
Ann Brinkmalm ◽  
Malin E. Andersson ◽  
Chen Gang ◽  
Gunnar Brinkmalm ◽  
...  

2008 ◽  
Vol 18 (3) ◽  
pp. 391-404 ◽  
Author(s):  
Jonathan D. Wood ◽  
Franziska Bonath ◽  
Shashvita Kumar ◽  
Christopher A. Ross ◽  
Vincent T. Cunliffe
Keyword(s):  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Mehmet Ilyas Cosacak ◽  
Christos Papadimitriou ◽  
Caghan Kizil

Regenerative capacity of the brain is a variable trait within animals. Aquatic vertebrates such as zebrafish have widespread ability to renew their brains upon damage, while mammals have—if not none—very limited overall regenerative competence. Underlying cause of such a disparity is not fully evident; however, one of the reasons could be activation of peculiar molecular programs, which might have specific roles after injury or damage, by the organisms that regenerate. If this hypothesis is correct, then there must be genes and pathways that (a) are expressed only after injury or damage in tissues, (b) are biologically and functionally relevant to restoration of neural tissue, and (c) are not detected in regenerating organisms. Presence of such programs might circumvent the initial detrimental effects of the damage and subsequently set up the stage for tissue redevelopment to take place by modulating the plasticity of the neural stem/progenitor cells. Additionally, if transferable, those “molecular mechanisms of regeneration” could open up new avenues for regenerative therapies of humans in clinical settings. This review focuses on the recent studies addressing injury/damage-induced molecular programs in zebrafish brain, underscoring the possibility of the presence of genes that could be used as biomarkers of neural plasticity and regeneration.


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