Acute ethyl acetate exposure suppresses spontaneous locomotor activity and exploration behaviour and impairs reference memory performance in rats: No evidence to support a role for L-type calcium channels

Abstract

Occupational exposure to volatile organic solvents has been reported to lead to hazardous effects. Ethyl acetate is a volatile organic compound used commonly in industry and found in many commercial products. The present study aimed to investigate the acute behavioural effects of ethyl acetate exposure in rats. The mechanism of its effects was further investigated by focusing on the possible involvement of L-type calcium channels. For this purpose, ethyl acetate (0.3 g/kg, i.p.) alone or concurrently with nimodipine (3 and 5 mg/kg, i.p.), a dihydropyridine calcium channel antagonist selective to L-type calcium channels, was administered to male Wistar albino rats. When compared to the saline control group, ethyl acetate significantly decreased the number of square-crossing, rearing, and sniffing in the open-field and impaired the reference memory performance in the three-panel runway. However, administration of nimodipine at the given doses did not block these effects of ethyl acetate. The findings suggest that L-type calcium channels may not contribute to the mechanism(s) responsible for the acute toxicity of ethyl acetate in rats regarding their central nervous system depression and memory disturbances although it should be more thoroughly investigated in further studies.