Depletion of cortical acetylcholine (ACh) correlates with reduced stimulus-evoked 2-deoxyglucose (2-DG) uptake in rodent somatosensory cortex. We examined the effect of unilateral basal forebrain lesions and subsequent cortical ACh depletion on (1) the ability of rats to detect a passively applied deflection of the whiskers, and (2) whisker- evoked 2-DG uptake. Normal adult rats were trained on a T-maze to respond by turning in one direction if the whiskers were displaced and in the opposite direction on presentation of a sham stimulus; only the left set of whiskers was stimulated. When the animal performed at the 80% correct level for three consecutive sessions (criterion), it was randomly assigned to a group receiving either a saline injection (sham lesion) or an ibotenic acid injection (excitotoxic lesion) into the right basal forebrain. Behavioral testing continued until the animal returned to the prelesion criterion, at which time a terminal 2-DG experiment was conducted. None of the sham-lesioned rats experienced disruption of their ability to perform the task. All excitotoxic basal forebrain-lesioned rats were impaired in task performance, but eventually returned to prelesion performance levels. The length of time required to return to criterion was positively correlated with the amount of cortical ACh depletion. Despite the behavioral recovery of the ACh-depleted rats, 2-DG uptake in response to whisker stimulation continued to be reduced in the somatosensory cortex ipsilateral to the basal forebrain lesion. These findings suggest that ACh depletion, which results in a long-lasting decrease in neuronal responses to evoked stimuli, transiently impairs an animal's ability to perceive and appropriately respond to sensory information; the duration of impairment is related to the degree of depletion.