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Drug-resistance and adverse effects of current drugs are the most obstacles in the treatment of epilepsy. In a plan for finding new natural anticonvulsant agents, we studied the anticonvulsant effects of essential oil (ZMEO) and methanolic extract (ZMME) of Zhumeria majdae in pentylene tetrazol (PTZ) and maximal electro-shock (MES) models in mice. Mice received different doses of ZMEO and ZMME, 30 min before induction of chemical and electrical convulsions. Neurotoxicity (movement toxicity and sedation) was evaluated using rota-rod test. The mortality was determined after 24 h following injection of different doses of the ZMEO and ZMME. The obtained results show that ZMEO dose-dependently protected mice from tonic convulsions induced by PTZ and MES with effective doses (ED) of 0.26 (0.13-0.39) and 0.27 (0.17-0.37) ml/kg respectively. Toxic doses (TD) in rota-rod test for ZMEO was 0.55 (0.42-0.70) ml/kg. ZMME at dose of 2 g/kg decreased tonic convulsions as much as 40 %. For ZMEO, TD of 0.55 (0.45-0.69) ml/kg was obtained. ZMME significantly decreased the walking time in rota-rod test at dose of 2 g/kg. Lethal dose (LD) of ZMEO was determined as 2.35 (1.98-2.65) ml/kg. ZMME showed about 34 % death of the animals at dose 5 g/kg. The essential oil of Z. majdae could be a good candidate for further anticonvulsive studies. [ABSTRACT FROM AUTHOR]

Rationale: Several reports have suggested the involvement of brain adenosine and dopamine receptors in different actions produced by ethanol such as motor incoordination or anxiolytic, hypnotic and reinforcing effects. The co-localization and interaction between adenosine and dopamine receptors in different brain regions has also been well documented. However, few studies have demonstrated the involvement of these mechanisms in the tolerance induced by ethanol. Objectives: The aim of the present study was to evaluate the role of adenosine and dopamine receptors in the development of rapid tolerance to ethanol-induced motor incoordination in mice. Methods: In connection with the rota-rod apparatus, the effects of acute administration of the adenosine receptor antagonists caffeine (non-selective), 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, adenosine A1 receptor antagonist) and 4-(2-[7- amino-2-{2-furyl}{1,2,4}triazolo-{2,3-a}{1,3,5}triazin-5-yl-amino] ethyl) phenol (ZM241385, adenosine A2A receptor antagonist), together with R(+)-7-cloro-8-hidroxi-3-metil-1-fenil-2,3,4,5-tetrahidro-1H-3-benzazepine (SCH23390, dopamine D1 receptor antagonist) and sulpiride (dopamine D2 receptor antagonist), alone or in combination with ethanol (2.25 g/kg, i.p.), were studied. Twenty-four hours after, all animals were re-tested on the rota-rod after receiving the same dose of ethanol. Results: The repeated administration of ethanol promoted a significant reduction of motor impairment on day 2 (i.e. rapid tolerance). This effect was blocked by caffeine (3.0--30.0 mg/kg, i.p.), DPCPX (3.0--6.0 mg/kg, i.p.) or SCH23390 (0.01--0.03 mg/kg, s.c.), but not with ZM241385 (0.5--1.0 mg/kg, i.p.) or sulpiride (1.0--3.0mg/kg, i.p.). Conclusions: Our results suggest that the rapid tolerance to ethanol-induced motor impairment in mice may be modulated by adenosine A1 receptors and dopamine D1 receptors. [ABSTRACT FROM AUTHOR]