Abstract
Organisms need to adapt to the ecological constraints in their habitat. How specific processes reflect such adaptations are difficult to model experimentally. We tested whether environmental shifts in oxygen tension lead to events in the adult newt brain that share features with processes occurring during neuronal regeneration under normoxia. By experimental simulation of varying oxygen concentrations, we show that hypoxia followed by re-oxygenation lead to neuronal death and hallmarks of an injury response, including activation of neural stem cells ultimately leading to neurogenesis. Neural stem cells accumulate reactive oxygen species (ROS) during re-oxygenation and inhibition of ROS biosynthesis counteracts their proliferation as well as neurogenesis. Importantly, regeneration of dopamine neurons under normoxia also depends on ROS-production. These data demonstrate a role for ROS-production in neurogenesis in newts and suggest that this role may have been recruited to the capacity to replace lost neurons in the brain of an adult vertebrate.
| Original language | English |
|---|---|
| Article number | e08422 |
| Number of pages | 16 |
| Journal | eLife |
| Volume | 4 |
| Early online date | 20 Oct 2015 |
| DOIs | |
| Publication status | Published - 16 Dec 2015 |
| Externally published | Yes |
Bibliographical note
Acknowledgements:We thank A Elewa, N Dantuma, C Sjögren for many helpful comments on the manuscript, and H Wang and M Kirkham for advice. This work was supported by grants from the European Research Council, Swedish Research Council, Swedish Cancer Society, AFA Insurances to AS. YC´s laboratory is supported by research grants from the Swedish Research Council, the Swedish Cancer Foundation, the Karolinska Institute Foundation, the Karolinska Institute distinguished professor award, the Torsten Soderbergs foundation, the NOVO Nordisk Foundation, the Advanced grant from the NOVO Nordisk foundation, and the Alice Wallenberg foundation
This article is distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use and redistribution provided that the original author and source are credited.
