According to a Pavlovian conditioning analysis, drug tolerance (in part) results from an association between cues present at the time of drug administration and the effect ofthe drug. Associations are enhanced by glucose administered after a conditioning trial, such enhancement being inversely related to the interval between the trial and glucose administration. If conditioning contributes to tolerance, glucose administered shortly after each drug administration should facilitate the acquisition of tolerance. Acquisition of tolerance was assessed both when glucose was administered shortly after each drug administration (immediate glucose) and when glucose was administered 24 h after each drug administration. As expected on the basis of the conditioning interpretation of tolerance, immediate glucose facilitated the acquisition of tolerance to the analgesic effect of morphine (Experiment 1) and the ataxic effect of ethanol (Experiment 2).Tolerance, a decrease in responsivity to a drug over the course of repeated administrations, can be affected by drug-associated cues. The contribution of drug-associated cues to tolerance is emphasized in a Pavlovian conditioning analysis of tolerance (see reviews by Dworkin, 1993;Ramsay & Woods, 1997; Siegel & Allan, 1998). Using the usual conditioning terminology, cues accompanying the primary drug effect function as conditioned stimuli (CSs). The direct effect of the drug constitutes the unconditioned stimulus (UCS). Prior to any learning, this pharmacological stimulation elicits responses that compensate for the drug-induced disturbances. These responses that compensate for the drug effect are unconditioned responses (UCRs). After some pairings of the predrug CS and pharmacological UCS, a drug-compensatory response is elicited as a conditioned response (CR). These drugcompensatory CRs mediate the development of tolerance by counteracting the drug effect.Consistent with the conditioning analysis, a variety of manipulations that attenuate the expression of conditional responding should also attenuate the acquisition of tolerance. Thus, in common with other CRs, the expression of drug tolerance is disrupted when a novel external stimulus is presented (external inhibition, see, e.g., Larson & Siegel, 1998;Siegel & Larson, 1996) or when the putative CS is altered (the context of drug administration changed, e.g., Epstein, Caggiula, Perkins, McKenzie, & Smith, 1991;Siegel, 1991). Even if the drug is reliably signaled by consistent environmental cues, the expression oftol-