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Neuroinflammation is associated with changes in glial mGluR5 expression and the development of neonatal excitotoxic lesions
Author(s) -
DrouinOuellet Janelle,
Brownell AnnaLiisa,
SaintPierre Martine,
Fasano Caroline,
Emond Vincent,
Trudeau LouisEric,
Lévesque Daniel,
Cicchetti Francesca
Publication year - 2011
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.21086
Subject(s) - neuroinflammation , ibotenic acid , neuroscience , astrogliosis , biology , glutamate receptor , nmda receptor , hippocampal formation , microglia , metabotropic glutamate receptor 5 , neurotoxin , lesion , gliosis , excitotoxicity , inflammation , metabotropic glutamate receptor , central nervous system , receptor , medicine , pathology , immunology , endocrinology , biochemistry
It has been hypothesized that neuroinflammation triggered during brain development can alter brain functions later in life. We investigated the contribution of inflammation to the alteration of normal brain circuitries in the context of neuroexcitotoxicity following neonatal ventral hippocampal lesions in rats with ibotenic acid, an NMDA glutamate receptor agonist. Excitotoxic ibotenic acid lesions led to a significant and persistent astrogliosis and microglial activation, associated with the production of inflammatory mediators. This response was accompanied by a significant increase in metabotropic glutamate receptor type 5 (mGluR5) expression within two distinct neuroinflammatory cell types; astrocytes and microglia. The participation of inflammation to the neurotoxin‐induced lesion was further supported by the prevention of hippocampal neuronal loss, glial mGluR5 expression and some of the behavioral perturbations associated to the excitotoxic lesion by concurrent anti‐inflammatory treatment with minocycline. These results indicate that neuroinflammation significantly contributes to long‐lasting excitotoxic effects of the neurotoxin and to some behavioral phenotypes associated with this model. Thus, the control of the inflammatory response may prevent the deleterious effects of excitotoxic processes that are triggered during brain development, limiting the risk to develop some of the behavioral manifestations related to these processes in adulthood. © 2010 Wiley‐Liss, Inc.