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Oxidative Medicine and Cellular Longevity
Volume 2015 (2015), Article ID 451512, 14 pages
Research Article

Nitric Oxide Regulates Neurogenesis in the Hippocampus following Seizures

1Center for Neuroscience and Cell Biology, Neuroendocrinology and Neurogenesis Group, University of Coimbra, 3004-517 Coimbra, Portugal
2Regenerative Medicine Program, Department of Biomedical Sciences and Medicine, University of Algarve, 8005-139 Faro, Portugal
3Center for Biomedical Research (CBMR), University of Algarve, 8005-139 Faro, Portugal

Received 30 April 2015; Accepted 18 May 2015

Academic Editor: Renata Santos

Copyright © 2015 Bruno P. Carreira et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Hippocampal neurogenesis is changed by brain injury. When neuroinflammation accompanies injury, activation of resident microglial cells promotes the release of inflammatory cytokines and reactive oxygen/nitrogen species like nitric oxide (NO). In these conditions, NO promotes proliferation of neural stem cells (NSC) in the hippocampus. However, little is known about the role of NO in the survival and differentiation of newborn cells in the injured dentate gyrus. Here we investigated the role of NO following seizures in the regulation of proliferation, migration, differentiation, and survival of NSC in the hippocampus using the kainic acid (KA) induced seizure mouse model. We show that NO increased the proliferation of NSC and the number of neuroblasts following seizures but was detrimental to the survival of newborn neurons. NO was also required for the maintenance of long-term neuroinflammation. Taken together, our data show that NO positively contributes to the initial stages of neurogenesis following seizures but compromises survival of newborn neurons.