Abstract:The effects of co-administration of caffeine and ethanol were assessed on the motor coordination of rats on the accelerating rotarod (accelerod). Ethanol (2.5 g/kg, orally) decreased motor performance on the accelerod. Co-administration of caffeine (5 and 20 mg/kg, orally) dose-dependently attenuated this ethanol-induced deficit. Caffeine (20 mg/kg, orally) alone did not affect motor performance in the test. As caffeine is a non-selective adenosine receptor antagonist the ability of adenosine A 1 and A 2A receptor blockade to attenuate ethanol-induced motor incoordination was determined. Pre-treatment with the adenosine A 1 receptor antagonist DPCPX (5 mg/kg, intraperitoneally) attenuated ethanol (2.5 g/ kg, orally)-induced motor incoordination. By contrast, prior administration of the adenosine A 2A selective antagonist SCH 58261 (10 mg/kg intraperitoneally) had no effect on the ethanol-induced motor deficit. These data demonstrate that adenosine A 1 receptor blockade mimics the inhibitory action of caffeine on ethanol-induced motor incorordination, and may contribute to the ability of caffeine to offset the acute intoxicating actions of ethanol.Ethanol and caffeine are widely consumed recreational drugs. Both are frequently taken in combination through mixing alcoholic and caffeinated beverages. Reasons for combining caffeine with ethanol may stem from the popular belief that caffeine can offset the acute intoxicating actions of ethanol, enhance the stimulatory properties and ameliorate hangover effects following excessive alcohol consumption. The mechanism(s) mediating such an interaction are not presently understood.
Umbelliferyloxymethyl phosphonates:non-chelating ionophores that A protect rat hippocampal cells from toxic Aβ42 B partition Zn from water to octanol C inhibit Zn promoted aggregation of Aβ42, D delay Zn signaling by FluoZin-3 in neuronal cells.
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