Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/67308
Title: Astroglia-microglia cross talk during neurodegeneration in the rat hippocampus
Author: Batlle, Montserrat
Ferri, Lorenzo
Andrade, Carmen
Ortega, Francisco Javier
Vidal Taboada, José Manuel
Pugliese, Marco
Mahy Gehenne, Josette Nicole
Rodríguez Allué, Manuel José
Keywords: Micròglia
Malalties neurodegeneratives
Rates (Animals de laboratori)
Microglia
Neurodegenerative Diseases
Rats as laboratory animals
Issue Date: 21-Apr-2015
Publisher: Hindawi
Abstract: Brain injury triggers a progressive inflammatory response supported by a dynamic astroglia-microglia interplay. We investigated the progressive chronic features of the astroglia-microglia cross talk in the perspective of neuronal effects in a rat model of hippocampal excitotoxic injury. N-Methyl-D-aspartate (NMDA) injection triggered a process characterized within 38 days by atrophy, neuronal loss, and fast astroglia-mediated S100B increase. Microglia reaction varied with the lesion progression. It presented a peak of tumor necrosis factor-α (TNF-α) secretion at one day after the lesion, and a transient YM1 secretion within the first three days. Microglial glucocorticoid receptor expression increased up to day 5, before returning progressively to sham values. To further investigate the astroglia role in the microglia reaction, we performed concomitant transient astroglia ablation with L-α-aminoadipate and NMDA-induced lesion. We observed a striking maintenance of neuronal death associated with enhanced microglial reaction and proliferation, increased YM1 concentration, and decreased TNF-α secretion and glucocorticoid receptor expression. S100B reactivity only increased after astroglia recovery. Our results argue for an initial neuroprotective microglial reaction, with a direct astroglial control of the microglial cytotoxic response. We propose the recovery of the astroglia-microglia cross talk as a tissue priority conducted to ensure a proper cellular coordination that retails brain damage.
Note: Reproducció del document publicat a: http://dx.doi.org/10.1155/2015/102419
It is part of: BioMed Research International, 2015, vol. 2015, p. 1-15
Related resource: http://dx.doi.org/10.1155/2015/102419
URI: http://hdl.handle.net/2445/67308
ISSN: 2314-6133
Appears in Collections:Articles publicats en revistes (Ciències Fisiològiques)

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