The FASEB Journal · 1996 · 150 citations · 0 references
MedicineNeurosciencePharmacologyEpilepsyNeurochemistryNeuropharmacologyCentral Nervous System ToxicityNeurochemical PharmacologyNeuroprotectionNeuroprotective PharmacologyNeurotoxic MechanismsNeurotoxicity MechanismsAntioxidant PropertiesAntioxidant TreatmentBrain ToxicityMelatonin PharmacologyMelatonin TreatmentNeuroprotective AgentsNeuroprotective AntioxidantsNeuroprotective Pharmacotherapy
In this study, we injected 10 mg/kg kainate i.p. into rats. This resulted in a brain injury, which we quantified in the hippocampus, the amygdala, and the pyriform cortex. Neuronal damage was preceded by a set of typical behavioral signs and by biochemical changes (noradrenaline decrease and 5‐hydroxyindoleacetic acid increase) in the af‐fected brain areas. Melatopin (2.5 mg/kg) was injected i.p. four times: 20 min before kainate, immediately after, and 1 and 2 h after the kainate. The cumulative dose of 10 mg/kg melatonin prevented kainate‐induced neuronal death as well as behavioral and biochemical disturbances. A possible mechanism of melatonin‐provided neuroprotection lies in its antioxidant action. Our results suggest that melatonin holds potential for the treatment of pathologies such as epilepsy‐associated brain damage, stroke, and brain trauma.—Giusti, P., Lipartiti, M., Franceschini, D., Schiavo, N., Floreani, M., Manev, H. Neuroprotection by melatonin from kainate‐induced excitotoxicity in rats. FASEB J. 10, 891‐896 (1996)