Table of Contents Author Guidelines Submit a Manuscript
Neural Plasticity
Volume 2014, Article ID 610343, 15 pages
Review Article

Surveillance, Phagocytosis, and Inflammation: How Never-Resting Microglia Influence Adult Hippocampal Neurogenesis

1Ikerbasque Foundation, 48011 Bilbao, Spain
2Achucarro Basque Center for Neuroscience, Bizkaia Science and Technology Park, 48170 Zamudio, Spain
3Department of Neurosciences, University of the Basque Country, 48940 Leioa, Spain
4Centre de Recherche du CHU de Québec, Axe Neurosciences, Canada G1P 4C7
5Département de Médecine Moléculaire, Université Laval, Canada G1V 4G2

Received 10 December 2013; Accepted 11 February 2014; Published 19 March 2014

Academic Editor: Carlos Fitzsimons

Copyright © 2014 Amanda Sierra 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.


Microglia cells are the major orchestrator of the brain inflammatory response. As such, they are traditionally studied in various contexts of trauma, injury, and disease, where they are well-known for regulating a wide range of physiological processes by their release of proinflammatory cytokines, reactive oxygen species, and trophic factors, among other crucial mediators. In the last few years, however, this classical view of microglia was challenged by a series of discoveries showing their active and positive contribution to normal brain functions. In light of these discoveries, surveillant microglia are now emerging as an important effector of cellular plasticity in the healthy brain, alongside astrocytes and other types of inflammatory cells. Here, we will review the roles of microglia in adult hippocampal neurogenesis and their regulation by inflammation during chronic stress, aging, and neurodegenerative diseases, with a particular emphasis on their underlying molecular mechanisms and their functional consequences for learning and memory.