1,8-cineole (CIN), found in many plant essential oils, exerts various pharmacological effects that many of them are mediated by direct or indirect interaction with ion channels as essential regulators of neuronal activity. In this study, the intracellular recording technique was employed to assess the effect of 1,8-cineoll on the electrical properties of the neurons within subesophageal ganglia of snail Caucasotachea atrolabiata. Extracellular application of CIN (3 mM) increased the frequency of spontaneous action potentials, reduced the slope of repolarization of action potentials and suppressed both duration and amplitude of afterhyperpolarization, suggesting an inhibition of outward potassium currents. Bath application of higher concentration of 1,8-cineoll (5 mM) slowly changed the pattern of activity from regular spiking to burst firing, which was associated by paroxysmal depolarization shift (PDS) and was reversible after washing out by normal Ringer. Burst firing and PDS was reduced by nifedipine (blocker of L-type calcium channels) and was eliminated in the presence of nickel chloride (nonspecific blocker of calcium channels), suggesting critical involvement of inward calcium currents in the modulatory action of CIN on neuronal activity. In many aspects, the neuronal activity in the presence of CIN resumed those induced after application of tetraethyl ammonium, which supports the scenario of an inhibition of potassium currents by CIN. H-89 (inhibitor of cAMP-dependent protein kinase) and chelerythrine (inhibitor of protein kinase C) were not able to significantly block CIN-induced burst firing and PDS, showing that the epileptogenic action of CIN is not critically dependent on ion channels phosphorylation.