Denis Bernabé

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The neuronal nuclei (NeuN) antigen is increasingly being used as a specific marker to identify neuronal cell loss under various pathological conditions. However, recent studies pointed out that a decrease in NeuN labeling could also be due to the reduction of protein expression level or loss of antigenicity and this was not necessarily related to neuronal(More)
To date, only short-term glial reaction has been extensively studied following soman or other warfare neurotoxicant poisoning. In a context of cell therapy by neural progenitor engraftment to repair brain damage, the long-term effect of soman on glial reaction and neural progenitor division was analyzed in the present study. The effect of soman poisoning(More)
Nerve agent poisoning is known to induce full-blown seizures, seizure-related brain damage (SRBD), and lethality. Effective and quick management of these seizures is critical. In conditions of delayed treatment, presently available measures are inadequate calling for optimization of therapeutic approaches. The effects of ketamine/atropine sulfate (KET/AS)(More)
We previously described that enhanced proliferation of neural progenitors occurred in the subgranular zone (SGZ) of the dentate gyrus and in the subventricular zone (SVZ) of the mouse brain following soman poisoning. Then, a discrete number of these cells seemed to migrate and engraft into the main damaged brain regions (hippocampus; septum and amygdala)(More)
Gliotic scar formation and angiogenesis are two biological events involved in the tissue reparative process generally occurring in the brain after mechanically induced injury, ischemia or cerebral tumor development. For the first time, in this study, neo-vascularization and glial scar formation were investigated in the brain of soman-poisoned mice over a(More)
Soman poisoning induces long-term neuropathology characterized by the presence of damaged neurons up to 2 months after exposure in various central brain areas, especially the hippocampal CA1 layer. Rapid depletion of this layer could therefore be expected. Surprisingly, the CA1 layer remained consistently visible, suggesting delayed death of these damaged(More)
The efficacy of aspirin and mefenamic acid to counteract soman-induced brain damage was investigated in mice. Neuronal damage was evaluated in the hippocampus and amygdala by performing omega3 receptor density measurements and hemalun-phloxin staining. The effect of both drugs on the proliferation of neural progenitors after soman exposure was also(More)
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