Ghasemi, F., Tamadon, H., Hosseinmardi, N., Janahmadi, M. (2018). Effects of Dorema ammoniacum Gum on Neuronal Epileptiform Activity-Induced by Pentylenetetrazole. Iranian Journal of Pharmaceutical Research, 17(2), 735-742.
Fatemeh Ghasemi; Hanieh Tamadon; Narges Hosseinmardi; Mahyar Janahmadi. "Effects of Dorema ammoniacum Gum on Neuronal Epileptiform Activity-Induced by Pentylenetetrazole". Iranian Journal of Pharmaceutical Research, 17, 2, 2018, 735-742.
Ghasemi, F., Tamadon, H., Hosseinmardi, N., Janahmadi, M. (2018). 'Effects of Dorema ammoniacum Gum on Neuronal Epileptiform Activity-Induced by Pentylenetetrazole', Iranian Journal of Pharmaceutical Research, 17(2), pp. 735-742.
Ghasemi, F., Tamadon, H., Hosseinmardi, N., Janahmadi, M. Effects of Dorema ammoniacum Gum on Neuronal Epileptiform Activity-Induced by Pentylenetetrazole. Iranian Journal of Pharmaceutical Research, 2018; 17(2): 735-742.
Effects of Dorema ammoniacum Gum on Neuronal Epileptiform Activity-Induced by Pentylenetetrazole
1Department of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Evin, Tehran, Iran.
2Neuroscience Research Center, Department of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Evin, Tehran, Iran.
Abstract
Epilepsy is a chronic neurological disease which disrupts the neuronal electrical activity. One-third of patients are resistant to treatment with available antiepileptic agents. The use of herbal medicine for treating several diseases including epilepsy is on the rise. Therefore, further investigation is required to verify the safety and effectiveness of Phytomedicine in treating diseases. The current study is an attempt to elucidate the electrophysiological mechanism of the effect of Dorema ammoniacum gumon a cellular model of epilepsy, using intracellular recording method. The gum was applied either after or before pentylenetetrazole, as an epileptic drug, in order to explore the possible therapeutic and preventive effects of gum. Treatment with D. ammoniacum gum alone increased the neuronal excitability and when applied before or after treatment with PTZ not only did not prevent or change the electrophysiological changes induced by PTZ but also re-enhanced the induction of hyperexcitability and epileptiform activity through depolarizing membrane potential, increasing the firing frequency and decreasing the AHP amplitude. However, phenobarbital, as a standard anti-epileptic agent, almost reversed the effect of PTZ and preserved the normal firing properties of F1 neurons. The possible candidate mechanism of the effect of gum on neuronal excitability could be suppressive effects of gum on voltage and/or Ca2+ dependent K+ channels currents underlying AHP.
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