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Anticonvulsant Effect of Melatonin Through Atp-Sensitive Channels in Mice Publisher Pubmed



Mohammadi F1 ; Shakiba S1, 2, 3 ; Mehrzadi S4 ; Afshari K1, 2, 3 ; Rahimnia AH1, 2, 3 ; Dehpour AR1, 2, 3
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Authors Affiliations
  1. 1. Brain and Spinal Cord Injury Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Experimental Medicine Research Center, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  4. 4. Razi Drug Research Center, Iran University of Medical Sciences, Shahid Hemmat Highway, Tehran, 1449614535, Iran

Source: Fundamental and Clinical Pharmacology Published:2020


Abstract

Melatonin is a neurohormone secreted principally by the pineal gland. This molecule has various pharmacological properties including improving immune system, prevent cancer, anti-aging, and anti-oxidant effects. The anticonvulsant effects of melatonin have been proved by previous studies. Adenosine triphosphate (ATP)-sensitive potassium (KATP) channels are considered as an important target in the seizure modulation. The aim of the present study was to investigate the anticonvulsant effect of melatonin in pentylenetetrazole (PTZ)-induced seizures in mice, focusing on its ability to regulate KATP channels. Acute intraperitoneal administration of melatonin (40 and 80 mg/kg) increased clonic seizure threshold induced by intravenous administration of PTZ. Melatonin (40 and 80 mg/kg) increased the latency of clonic seizure and reduced its frequency in mice receiving an intraperitoneal injection of PTZ. Administration of glibenclamide, a KATP channels blocker, before intravenous injection of PTZ reduced melatonin anticonvulsant effect. Diazoxide and cromakalim, as KATP channels openers, increased antiseizure effect of melatonin in PTZ model of seizures. These findings suggest that the antiseizure effect of melatonin probably is gained through increasing the opening of KATP channels. © 2019 Societe Francaise de Pharmacologie et de Therapeutique
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