Glial fibrillary acidic protein (GFAP)+ cells give rise to new neurons in the neurogenic niches; whether they are able to generate neurons in the cortical parenchyma is not known. Here, we use genetic fate mapping to examine the progeny of GFAP+ cells after postnatal hypoxia, a model for the brain injury observed in premature children. Following hypoxia, immature cortical astroglia underwent a shift towards neuronal fate and generated cortical excitatory neurons that appeared synaptically integrated into the circuitry. Fate mapped cortical GFAP+ cells derived ex vivo from hypoxic, but not normoxic mice were able to form pluripotent, long-term self-renewing neurospheres. Similarly, exposure to low oxygen conditions in vitro induced stem cell-like potential in immature cortical GFAP+ cells. Our data support the conclusion that hypoxia promotes pluripotency in GFAP+ cells in the cortical parenchyma. Such plasticity possibly explains the cognitive recovery found in some preterm children.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.