ArticleMolecular neurobiology2022
Melatonin Pretreatment Protects Against Status epilepticus, Glutamate Transport, and Oxidative Stress Induced by Kainic Acid in Zebrafish.
Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Melatonin Modulates Behavioral and Physiological Responses in a Concentration-dependent Manner in a Pilocarpine-induced Seizure-like Model Using Zebrafish Larvae.Neurotoxicity research · 2026Article
- Clinical daily rhythms of seizure in different subtypes of temporal lobe epilepsy.Frontiers in neurology · 2025Article
- Effect of Levetiracetam on Oxidant-Antioxidant Activity during Long-Term Temporal Lobe Epilepsy in Rats.International journal of molecular sciences · 2024Article
- Melatonin regulates microglial polarization to M2 cell via RhoA/ROCK signaling pathway in epilepsy.Immunity, inflammation and disease · 2023Article
- Melatonin modulates the hypothalamic-pituitary neuroendocrine axis to regulate physiological color change in teleost fish.International journal of biological sciences · 2023Article
- An aqueous extract of Syzygium cumini protects against kainate-induced status epilepticus and amnesia: evidence for antioxidant and anti-inflammatory intervention.Metabolic brain disease · 2022Article
- Melatonin pretreatment on exosomes: Heterogeneity, therapeutic effects, and usage.Frontiers in immunology · 2022Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
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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