6533b830fe1ef96bd1297069

RESEARCH PRODUCT

Time-dependent contribution of non neuronal cells to BDNF production after ischemic stroke in rats.

Yannick BéjotMaurice GiroudAnne Prigent-tessierAnne Prigent-tessierClaire CachiaPhilippe GarnierPhilippe GarnierNathalie BertrandNathalie BertrandChristine MarieChristine MarieClaude MossiatClaude Mossiat

subject

MaleTime Factorsmedicine.medical_treatmentCentral nervous systemIschemiaBDNF productionFunctional LateralityBrain IschemiaBrain ischemia03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineNeurotrophic factorsGlial Fibrillary Acidic ProteinmedicineAnimalsRats WistarStrokeCellular localization030304 developmental biologyBrain-derived neurotrophic factorBrain ChemistryNeurons0303 health sciencesbusiness.industryBDNF localization[SCCO.NEUR]Cognitive science/NeuroscienceBrain-Derived Neurotrophic Factor[SCCO.NEUR] Cognitive science/NeuroscienceBrainCell BiologyCerebral Infarctionmedicine.diseaseRatsStrokemedicine.anatomical_structurenervous systemIntracranial Embolism[ SCCO.NEUR ] Cognitive science/NeurosciencebusinessStroke recoveryNeuroscience030217 neurology & neurosurgery

description

International audience; Although brain-derived neurotrophic factor (BDNF) plays a central role in recovery after cerebral ischemia, little is known about cells involved in BDNF production after stroke. The present study testes the hypothesis that neurons are not the unique source of neosynthesized BDNF after stroke and that non neuronal-BDNF producing cells differ according to the delay after stroke induction. For this purpose, cellular localization of BDNF and BDNF content of each hemisphere were analysed in parallel before and after (4h, 24h and 8d) ischemic stroke in rats. Stroke of different severities was induced by embolization of the brain with variable number of calibrated microspheres allowing us to explore the association between BDNF production and neuronal death severity. The main results are that (a) unilateral stroke increased BDNF production in both hemispheres with a more intense and long-lasting effect in the lesioned hemisphere, (b) BDNF levels either of the lesioned or unlesioned hemispheres were not inversely correlated to neuronal death severity whatever the delay after stroke onset, (c) in the unlesioned hemisphere, stroke resulted in increased BDNF staining in neurons and ependymal cells (at 4h and 24h), (d) in the lesioned hemisphere, beside neurons and ependymal cells, microglial cells (at 24h), endothelial cells of cerebral arterioles (at 4h and 24h) and astrocytes (at 8d) exhibited a robust BDNF staining as well. Taken together, overall data suggest that non neuronal cells are able to produce substantial amount of BDNF after ischemic stroke and that more attention should be given to these cells in the design of strategies aimed at improving stroke recovery through BDNF-related mechanisms.

10.1016/j.neuint.2010.10.019https://pubmed.ncbi.nlm.nih.gov/21074587