The Electrophysiological Consequences of Artemisia dracunculus L. (Tarragon) Extract on Pentylenetetrazol-Induced Epileptiform Activity in Snail Neurons

Document Type : Original Article


1 Neuroscience Research Center and Department of Physiology, Medical School, Shahid Beheshti Medical Sciences University, Tehran, Iran

2 Department of Biology, College of Sciences, Shiraz University, Shiraz, Iran

3 Department of Plant Protection, Faculty of Agricultural Sciences, Shahed University, Tehran, Iran

4 Department of Pharmacognosy, Shahid Beheshti University of Medical Sciences, Tehran, Iran


Objective: Plant extracts are of considerable interest because of their antiepileptic activities. However, the mechanisms of action are not clearly defined.
Materials and Methods: Here, the effects of Artemisia dracunculus L. (tarragon) leaves extract on excitability and electrophysiological characteristics of snail neurones were investigated, using an intracellular recording technique.
Results: Application of tarragon extract (0.05%) resulted in complete disappearance of paroxysmal depolarization shift (PDS) as elicited by pentylenetetrazol (PTZ), an epileptogenic drug. It also significantly decreased the firing frequency and shifted the firing pattern from bursting in the presence of PTZ to an irregular doublet activity. Changes in excitability properties were associated with a significant increase and decrease in the duration of action potential, and in the amplitude of after-hyperpolarization (AHP), respectively. When tarragon extract was applied alone, spontaneous activity became irregular and was interrupted by large inhibitory postsynaptic potentials (IPSPs), which disappeared following application of picrotoxin (100 μM). Tarragon also caused a significant decrease both in the amplitude of action potentials and AHP, and broadened the action potentials. However, pretreatment with extract did not prevent the induction of
epileptiform activity by PTZ.
Conclusion: The findings suggest that tarragon extract may affect membrane ion channels and/or GABAA receptors leading to a reduction in neuronal excitability.