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Stab wound injury of the zebrafish telencephalon: A model for comparative analysis of reactive gliosis
Author(s) -
Baumgart Emily Violette,
Barbosa Joana S.,
Ballycuif Laure,
Götz Magdalena,
Ninkovic Jovica
Publication year - 2012
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.22269
Subject(s) - zebrafish , biology , cerebrum , neurogenesis , microglia , gliosis , glial scar , neuroglia , neuroscience , parenchyma , astrogliosis , pathology , astrocyte , anatomy , central nervous system , inflammation , immunology , medicine , biochemistry , botany , gene
Reactive glia, including astroglia and oligodendrocyte progenitors (OPCs) are at the core of the reaction to injury in the mammalian brain with initially beneficial and later partially adverse functions such as scar formation. Given the different glial composition in the adult zebrafish brain with radial ependymoglia but no parenchymal astrocytes, we examined the glial response to an invasive stab wound injury model in the adult zebrafish telencephalon. Strikingly, already a few days after injury the wound was closed without any scar tissue. Similar to mammals, microglia cells reacted first and accumulated close to the injury site, while neither GFAP+ radial ependymoglia nor adult OPCs were recruited to the injury site. Moreover, OPCs failed to increase their proliferation after this injury, while the number of proliferating GFAP+ glia was increased until 7 days after injury. Importantly, neurogenesis was also increased after injury, generating additional neurons recruited to the parenchyma which survived for several months. Thus, these data suggest that the specific glial environment in the adult zebrafish telencephalon is not only permissive for long‐term neuronal survival, but avoids scar formation. Invasive injury in the adult zebrafish telencephalon may therefore provide a useful model to untangle the molecular mechanisms involved in these beneficial glial reactions. © 2011 Wiley Periodicals, Inc.