Premium
Light regulates the expression of the BDNF/TrkB system in the adult Zebrafish retina
Author(s) -
SánchezRamos C.,
BonninArias C.,
Guerrera M.C.,
Calavia M.G.,
Chamorro E.,
Montalbano G.,
LópezVelasco S.,
LópezMuñiz A.,
Germanà A.,
Vega J.A.
Publication year - 2013
Publication title -
microscopy research and technique
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 118
eISSN - 1097-0029
pISSN - 1059-910X
DOI - 10.1002/jemt.22133
Subject(s) - tropomyosin receptor kinase b , zebrafish , immunostaining , retina , brain derived neurotrophic factor , biology , darkness , neurotrophin , neurotrophic factors , microbiology and biotechnology , neuroscience , receptor , immunohistochemistry , immunology , genetics , gene , botany
The retina of the adult zebrafish express brain‐derived neurotrophic factor (BDNF) and its signaling receptor TrkB. This functional system is involved in the biology of the vertebrate retina and its expression is regulated by light. This study was designed to investigate the effects of cyclic (12 h light/12 h darkness) or continuous (24 h) exposure during 10 days to white light, white‐blue light, and blue light, as well as of darkness, on the expression of BDNF and TrkB in the retina. BDNF and TrkB were assessed in the retina of adult zebrafish using quantitative real‐time polymerase chain reaction and immunohistochemistry. Exposure to white, white‐blue, and blue light causes a decrease of BDNF mRNA and of BDNF immunostaining, independently of the pattern of light exposition. Conversely, in the same experimental conditions, the expression of TrkB mRNA was upregulated and TrkB immunostaining increased. Exposition to darkness diminished BDNF and TrkB mRNAs, and abolished the immunostaining for BDNF but not modified that for TrkB. These results demonstrate the regulation of BDNF and TrkB by light in the retina of adult zebrafish and might contribute to explain some aspects of the complex pathophysiology of light‐induced retinopathies. Microsc. Res. Tech., 2013. © 2012 Wiley Periodicals, Inc.