Research in Medicine

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Abdollahi R, Hosseinmardi N, Janahmadi M. Effect of melatonin on electrophysiological parameters in an epileptic model by pentylenetetrazole. Research in Medicine 2021; 45 (2) :1-5
URL: http://pejouhesh.sbmu.ac.ir/article-1-2171-en.html

Background: Epilepsy is one of the most common neurological diseases in the world. Intracellular recording from neurons with epileptiform activity has well shown the burst firing pattern. Previous studies have shown that melatonin anti-epileptic effects, although effective on the neuronal properties and alteration of the firing pattern, has not been determined yet. Therefore, in the present study, we investigated the effect of melatonin on the electrophysiological parameters in an epileptic model induced by pentylenetetrazole (PTZ). 
Methods and materials: An experimental study was performed on the soma membrane of F1 neurons of sub-esophageal ganglia of Helix aspersa (Iranian garden snail). The firing pattern and action potential were recorded using a single electrode intracellular recording under controlled conditions. The epileptiform activity was induced using pentylenetetrazole and treatment was done using melatonin (100μM). Data analysis was carried out using Prism (version 8, GraphPad Software,Inc.) running one-way ANOVA followed by Tukey’s test. 
Results: Melatonin significantly prevented the depolarizing effect of pentylenetetrazole on resting membrane potential at concentration of 100μM (P<0.001). In addition, it caused a significant (P<0.001) reduction in firing frequency and an increase in the afterhyperpolarization potential.Furthermore, it resulted in changes in the electrical firing activity of neurons from bursting in the present of PTZ to a tonic firing in the control condition.
Conclusions: It seems that, by altering the electrophysiological parameters, melatonin caused a reduction of epileptiform activity and changed the bursting pattern due to PTZ to a tonic pattern. Thus, it can be concluded that melatonin can be effective in the treatment of epilepsy by reducing neuronal excitability.