Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/97691
Title: Blockade of microglial KATP-channel abrogates suppression of inflammatory-mediated inhibition of neural precursor cells
Author: Ortega, Francisco J.
Vukovic, J.
Rodríguez Allué, Manuel José
Bartlett, P.F.
Keywords: Inflamació
Micròglia
Neurobiologia del desenvolupament
Rates (Animals de laboratori)
Inflammation
Microglia
Developmental neurobiology
Rats as laboratory animals
Issue Date: 6-Dec-2013
Publisher: Wiley
Abstract: Microglia positively affect neural progenitor cell physiology through the release of inflammatory mediators or trophic factors. We demonstrated previously that reactive microglia foster K(ATP) -channel expression and that blocking this channel using glibenclamide administration enhances striatal neurogenesis after stroke. In this study, we investigated whether the microglial K(ATP) -channel directly influences the activation of neural precursor cells (NPCs) from the subventricular zone using transgenic Csf1r-GFP mice. In vitro exposure of NPCs to lipopolysaccharide and interferon-gamma resulted in a significant decrease in precursor cell number. The complete removal of microglia from the culture or exposure to enriched microglia culture also decreased the precursor cell number. The addition of glibenclamide rescued the negative effects of enriched microglia on neurosphere formation and promoted a ∼20% improvement in precursor cell number. Similar results were found using microglial-conditioned media from isolated microglia. Using primary mixed glial and pure microglial cultures, glibenclamide specifically targeted reactive microglia to restore neurogenesis and increased the microglial production of the chemokine monocyte chemoattractant protein-1 (MCP-1). These findings provide the first direct evidence that the microglial K(ATP) -channel is a regulator of the proliferation of NPCs under inflammatory conditions.
Note: Versió postprint del document publicat a: http://dx.doi.org/10.1002/glia.22603
It is part of: Glia, 2013, vol. 62, num. 2, p. 247-258
Related resource: http://dx.doi.org/10.1002/glia.22603
URI: http://hdl.handle.net/2445/97691
ISSN: 0894-1491
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)

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