Melatonin Pretreatment Protects Against Status Epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish
Autor: | Ana Caroline Salvador de Farias, Samira Leila Baldin, Eduardo Ronconi Dondossola, Eduardo Pacheco Rico, Henrique Teza Bernardo, Karolyne de Pieri Pickler |
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Rok vydání: | 2021 |
Předmět: |
Kainic acid
Amino Acid Transport System X-AG Neuroscience (miscellaneous) Glutamic Acid Status epilepticus Pharmacology medicine.disease_cause Neuroprotection Antioxidants Melatonin Superoxide dismutase Cellular and Molecular Neuroscience chemistry.chemical_compound Epilepsy Status Epilepticus medicine Animals Zebrafish Neurons Kainic Acid biology Superoxide Dismutase Chemistry Glutamate receptor Catalase medicine.disease Glutathione Oxidative Stress Neuroprotective Agents Neurology biology.protein medicine.symptom Reactive Oxygen Species Oxidative stress medicine.drug |
Popis: | Status epilepticus (SE) develops from abnormal electrical discharges, resulting in neuronal damage. Current treatments include antiepileptic drugs. However, the most common drugs used to treat seizures may sometimes be ineffective and have many side effects. Melatonin is an endogenous physiological hormone that is considered an alternative treatment for neurological disorders because of its free radical scavenging property. Thus, this study aimed to determine the effects of melatonin pretreatment on SE by inducing glutamatergic hyperstimulation in zebrafish. Seizures were induced in zebrafish using kainic acid (KA), a glutamate analog, and the seizure intensity was recorded for 60 min. Melatonin treatment for 7 days showed a decrease in seizure intensity (28%), latency to reach score 5 (14 min), and duration of SE (29%). In addition, melatonin treatment attenuated glutamate transporter levels, which significantly decreased in the zebrafish brain after 12 h of KA-induced seizures. Melatonin treatment reduced the increase in oxidative stress by reactive oxygen species formation through thiobarbituric acid reactive substances and 2‘,7‘-dichiorofluorescin, induced by KA-seizure. An imbalance of antioxidant enzyme activities such as superoxide dismutase and catalase was influenced by melatonin and KA-induced seizures. Our study indicates that melatonin promotes a neuroprotective response against the epileptic profile in zebrafish. These effects could be related to the modulation of glutamatergic neurotransmission, recovery of glutamate uptake, and oxidative stress parameters in the zebrafish brain. |
Databáze: | OpenAIRE |
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