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Microglia and neuronal cell death

Published online by Cambridge University Press:  01 March 2012

José L. Marín-Teva*
Affiliation:
Departamento de Biología Celular, Facultad de Ciencias, Universidad de Granada, Granada, Spain
Miguel A. Cuadros
Affiliation:
Departamento de Biología Celular, Facultad de Ciencias, Universidad de Granada, Granada, Spain
David Martín-Oliva
Affiliation:
Departamento de Biología Celular, Facultad de Ciencias, Universidad de Granada, Granada, Spain
Julio Navascués
Affiliation:
Departamento de Biología Celular, Facultad de Ciencias, Universidad de Granada, Granada, Spain
*
Correspondence should be addressed to: José L. Marín-Teva, Departamento de Biología Celular, Facultad de Ciencias, Universidad de Granada, E-18071 Granada, Spain phone: +34-958-246335; +34-958-243258 email: [email protected]

Abstract

Microglia, the brain's innate immune cell type, are cells of mesodermal origin that populate the central nervous system (CNS) during development. Undifferentiated microglia, also called ameboid microglia, have the ability to proliferate, phagocytose apoptotic cells and migrate long distances toward their final destinations throughout all CNS regions, where they acquire a mature ramified morphological phenotype. Recent studies indicate that ameboid microglial cells not only have a scavenger role during development but can also promote the death of some neuronal populations. In the mature CNS, adult microglia have highly motile processes to scan their territorial domains, and they display a panoply of effects on neurons that range from sustaining their survival and differentiation contributing to their elimination. Hence, the fine tuning of these effects results in protection of the nervous tissue, whereas perturbations in the microglial response, such as the exacerbation of microglial activation or lack of microglial response, generate adverse situations for the organization and function of the CNS. This review discusses some aspects of the relationship between microglial cells and neuronal death/survival both during normal development and during the response to injury in adulthood.

Type
Research Article
Copyright
Copyright © Cambridge University Press 2012

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