Paroxysmal 7- to 12-Hz high-voltage rhythmic spike (HVRS) or spike-wave discharges often appear in several particular strains of rats. However, functional hypotheses of these 7-12 Hz high-voltage cortical oscillations (absence seizure vs. idling mu rhythm) are inconclusive. The mu rhythm can be provoked by flicker stimulation (FS) in most people, but FS is less effective at eliciting absence epileptic activity. Therefore FS and antiepileptic drugs were used to verify the role of HVRS activity in Long-Evans rats with spontaneous HVRS discharges and Wistar rats without spontaneous HVRS discharges. The occurrence of HVRS discharges was significantly reduced by antiabsence drugs (ethosuximide, valproic acid, and diazepam) in dose-dependent manners, but high-dose carbamazepine displayed little effect. On the other hand, oscillation frequencies and durations of spontaneous HVRS discharges were not altered by FS. Under asynchronous brain activity, many FSs (>60%) elicited small-amplitude mu-rhythm-like activity in the barrel cortex concomitant with FS-related rhythms in the occipital cortex and resulted in significant augmentation of 7-12 Hz power in the parietal region. Furthermore, a large portion of FSs (>60%) revealed increase of 7-12 Hz power of the parietal cortex after ethosuximide administration (100 mg/kg ip) in Long-Evans rats. Similar FS-elicited phenomena also appeared in Wistar rats. Characteristics of FS-elicited mu-rhythm-like activities were consistent with those observed in humans, and they remarkably differed from those of spontaneous HVRS discharges. These results support the hypothesis that HVRS activity in Long-Evans rats may be an absence-like seizure activity rather than the mu rhythm.