Heliyon · 2019 · 32 citations · 30 references
PharmacyNeurobiologyNeuroscienceNeurochemistryNeuropharmacologyNeurotoxicologyCentral Nervous System ToxicityMultiple SclerosisNeurochemical PharmacologyNeuroprotectionNeurotoxic MechanismsNeurotoxicity MechanismsBehavioral Neurotoxicity TestingBrain ToxicityGlutathione Peroxidase ActivityNeurobehavioral AlterationsNeurotoxic Plant CompoundsOpen-field TestOxidative Stress InjuryRodent Neurotoxicology
, in mitigating the damaging effects of cuprizone on behaviour and the hippocampus. Twenty-four male albino mice aged 6-8 weeks were categorised into 4 equal groups: Group A (Control) received regular diet; Group B received 200 mg/kg/d of kolaviron in addition to their regular diet; Group C received 0.2% cuprizone diet only, while Group D received both kolaviron and cuprizone diet. The treatment lasted for 35 days after which behavioural tests (Morris water maze, Y maze and open field tests) were conducted and brain tissues were processed for histology, histochemistry (Nissl staining), immunohistochemistry (glial fibrillary acidic protein) and biochemistry (malondialdehyde, superoxide dismutase and glutathione peroxidase). Results showed that cuprizone toxicity led to weight loss, impairment in memory and exploratory drive, oxidative stress, chromatolysis and reactive astrocytosis; meanwhile administration of kolaviron prevented cuprizone-induced weight loss, memory decline, oxidative stress and neuromorphological alterations. In conclusion, administration of kolaviron might be useful in limiting the effects of cuprizone toxicity on the morphology and functions of the hippocampus.
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Mitochondrial defects in acute multiple sclerosis lesions
Don Mahad, Iryna Ziabreva, Hans Lassmann et al. · Brain · 2008 · 404 citations · Full text