Performance on delayed matching-to-position as a function of ethanol was investigated in rats and dose effects assessed by fitting an exponential decay model of forgetting to signal detection sensitivity scores. Three ethanol doses (0.25, 0.50, and 0.75 g/kg) and one isovolume saline control were examined. For further comparison, one dose of chlordiazepoxide (CDP; 5 mg/kg) and its saline control were also given. Forgetting functions were reasonably well described by the decay model under all treatment conditions. In addition, the functions's decay constant (-b) proved to be differentially sensitive to both drug and dose effects. Reduced decay estimates were obtained following the two lowest ethanol doses, the reduction being statistically significant for the 0.25 g/kg dose. In contrast, the function estimate of initial sensitivity, the intercept parameter (SI0), was not significantly affected by ethanol. Consistent with the low-dose ethanol effects, CDP significantly decreased the value of the decay parameter while leaving the intercept parameter unaffected. But unlike ethanol, the variance accounted for by the model for the individual data was less following CDP administration. Drug effects were interpreted using the exponential decay model of forgetting, and the results suggest independent discriminative control over SI0 and b. The significant effect of the low-dose sedative-hypnotics upon b, with no attendant effects upon SI0, is suggested to result from enhanced, spontaneous, delay interval mediation.