Subacute administration of fluoxetine prevents short-term brain hypometabolism and reduces brain damage markers induced by the lithium-pilocarpine model of epilepsy in rats

Serotonin Depletion Does not Modify the Short-Term Brain Hypometabolism and Hippocampal Neurodegeneration Induced by the Lithium–Pilocarpine Model of Status Epilepticus in Rats

“…When evaluated by [ 18 F]FDG PET, lithium-pilocarpine triggered an intense and widespread brain hypometabolism not just restricted to hippocampus or temporal lobes, as reported by our group and others (Goffin et al 2009;Guo et al 2009;Lee et al 2012;Shiha et al 2015). Despite the superb sensitivity of PET, the latter can be explained by the physical and technical limits of the current PET cameras (Moses 2011).…”

“…Six animals per group were used for the histochemical experiments. For Fluoro-Jade C staining, we followed the protocol originally reported by Schmued et al (2005) with minor modifications (Shiha et al 2015). Double labeling was achieved by incubating Cell Mol Neurobiol the slices in a 0.0001 % Fluoro-Jade C/0.001 % DAPI solution.…”

“…To evaluate the brain metabolic activity, [ 18 F]FDG PET imaging was performed 3 days after pilocarpine administration, as previously reported (Shiha et al 2015). Briefly, rats fasted for at least 12 h were injected with the positron emitter radiopharmaceutical [ 18 F]FDG (approx.…”

“…Double labeling was achieved by incubating Cell Mol Neurobiol the slices in a 0.0001 % Fluoro-Jade C/0.001 % DAPI solution. GFAP immunohistochemistry was carried out by a one-step technique using a fluorescent-labeled anti-GFAP antibody (Sigma-Aldrich, St. Louis, MO) as described (Shiha et al 2015). The brain sections were visualized under fluorescence microscopy (Olympus IX51, Olympus Europa Holding, Germany).…”

“…Brain hypometabolism has been described to appear shortly after the SE onset, returning the metabolic activity to baseline values in the subacute period (Lee et al 2012). Recently, we reported that short-term treatment with the selective 5-HT reuptake inhibitor (SSRI) fluoxetine prevented the acute hypometabolism (measured 3 days after the SE onset) and reduced the medium-term brain damage (evaluated on day 33), induced by lithium-pilocarpine administration in the latent phase of epileptogenesis (Shiha et al 2015). In particular, at the level of the hippocampus, subacute administration of fluoxetine diminished the number of neurodegenerating neurons (Fluoro-Jade C staining), reactive gliosis (GFAP immunohistochemistry) and apoptosis (caspase-9 immunohistochemistry).…”