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Melatonin Pretreatment Protects Against Status epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish.
Mol Neurobiol. 2022 Jan; 59(1):266-275.MN

Abstract

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.

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Authors+Show Affiliations

de Farias ACS
Translational Psychiatry Laboratory, Laboratory of Translational Biomedicine Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.
de Pieri Pickler K
Translational Psychiatry Laboratory, Laboratory of Translational Biomedicine Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.
Bernardo HT
Translational Psychiatry Laboratory, Laboratory of Translational Biomedicine Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.
Baldin SL
Translational Psychiatry Laboratory, Laboratory of Translational Biomedicine Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.
Dondossola ER
Translational Psychiatry Laboratory, Laboratory of Translational Biomedicine Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil.
Rico EP
Translational Psychiatry Laboratory, Laboratory of Translational Biomedicine Laboratory, Graduate Program in Health Sciences, University of Southern Santa Catarina (UNESC), Criciúma, Santa Catarina, Brazil. eduprico@gmail.com.

MeSH

Amino Acid Transport System X-AGAnimalsAntioxidantsCatalaseGlutamic AcidGlutathioneKainic AcidMelatoninNeuronsNeuroprotective AgentsOxidative StressReactive Oxygen SpeciesStatus EpilepticusSuperoxide DismutaseZebrafish

Pub Type(s)

Journal Article

Language

eng

PubMed ID

34665406

Citation

de Farias, Ana Caroline Salvador, et al. "Melatonin Pretreatment Protects Against Status Epilepticus, Glutamate Transport, and Oxidative Stress Induced By Kainic Acid in Zebrafish." Molecular Neurobiology, vol. 59, no. 1, 2022, pp. 266-275.
de Farias ACS, de Pieri Pickler K, Bernardo HT, et al. Melatonin Pretreatment Protects Against Status epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish. Mol Neurobiol. 2022;59(1):266-275.
de Farias, A. C. S., de Pieri Pickler, K., Bernardo, H. T., Baldin, S. L., Dondossola, E. R., & Rico, E. P. (2022). Melatonin Pretreatment Protects Against Status epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish. Molecular Neurobiology, 59(1), 266-275. https://doi.org/10.1007/s12035-021-02579-4
de Farias ACS, et al. Melatonin Pretreatment Protects Against Status Epilepticus, Glutamate Transport, and Oxidative Stress Induced By Kainic Acid in Zebrafish. Mol Neurobiol. 2022;59(1):266-275. PubMed PMID: 34665406.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Melatonin Pretreatment Protects Against Status epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish. AU - de Farias,Ana Caroline Salvador, AU - de Pieri Pickler,Karolyne, AU - Bernardo,Henrique Teza, AU - Baldin,Samira Leila, AU - Dondossola,Eduardo Ronconi, AU - Rico,Eduardo Pacheco, Y1 - 2021/10/19/ PY - 2021/06/09/received PY - 2021/09/24/accepted PY - 2021/10/20/pubmed PY - 2022/4/1/medline PY - 2021/10/19/entrez KW - Epilepsy KW - Glutamate KW - Melatonin KW - Oxidative stress KW - Zebrafish SP - 266 EP - 275 JF - Molecular neurobiology JO - Mol Neurobiol VL - 59 IS - 1 N2 - 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. SN - 1559-1182 UR - https://www.unboundmedicine.com/medline/citation/34665406/Melatonin_Pretreatment_Protects_Against_Status_epilepticus_Glutamate_Transport_and_Oxidative_Stress_Induced_by_Kainic_Acid_in_Zebrafish_ DB - PRIME DP - Unbound Medicine ER -