Acetate is the primary product of ethanol catabolism and can accumulate in the blood at concentrations of up to 2 mM following ethanol consumption. It has been suggested that some of the pharmacological actions of ethanol are mediated via acetate, which can lead indirectly to the release of endogenous adenosine. In the present experiments this hypothesis was tested by examining the effects of exogenous sodium acetate on the physiology of hippocampal slices from rat brain. Acetate had no significant effect on intracellular responses recorded from CA1 pyramidal neurons or on extracellular field potentials evoked from the either the CA1 region or the dentate gyrus. There was also no significant difference in responses to the adenosine receptor antagonist theophylline in CA1 pyramidal neurons recorded using intracellular filling solutions containing potassium acetate, KCl, or potassium methylsulfate. These results suggest that the presence of acetate, either in the extracellular medium or within an intracellular electrode, does not induce a significant increase in adenosine receptor activation in the hippocampus.