Background We previously demonstrated that acute and chronic treatment with ethanol (EtOH), respectively, decelerated and accelerated the propagation of cortical spreading depression (CSD) in rats and that the antioxidant carotenoid astaxanthin counteracted these effects. Here, we investigated whether noncarotenoid antioxidants exert the same action by testing α‐tocopherol in rats of various ages, with and without 5 to 10 days of EtOH abstinence. Methods Male Wistar young adult (60 to 80 days old) and mature adult (150 to 180 days old) rats received per gavage acute (1 day) or chronic (21 days) treatment with 3 g/kg/d EtOH combined with acute (300 mg/kg) or chronic (85 mg/kg/d) treatment with α‐tocopherol or vehicle‐only treatment (olive oil and water for α‐tocopherol and EtOH, respectively). CSD was recorded over 4 hours and the velocity of CSD propagation was calculated. On both ages, animals under chronic EtOH treatment were subjected to CSD recording immediately after EtOH treatment or after a 5‐ to 10‐day period of EtOH abstinence. Results In both age groups, acute and chronic EtOH exposure decelerated and accelerated CSD, respectively, versus the corresponding control groups. Addition of α‐tocopherol counteracted the effects of EtOH on CSD, returning CSD velocities to levels in control groups (p < 0.05). Chronic α‐tocopherol (85 mg/kg/d) did not alter CSD. Conclusions Our data reinforce the counteracting role of antioxidants on brain processes involved in the action of EtOH on CSD and suggest that this role is not a particular property of carotenoids; furthermore, this general feature of antioxidants is not substantially influenced by age or by 5 to 10 days of EtOH abstinence. Recordings of direct current potential change of cortical spreading depression (CSD) in five young adult and five mature adult rats representative of the following groups: naïve (no treatment), tocopherol, acute ethanol, chronic ethanol, and ethanol + tocopherol. Vertical dashed lines indicate the latency for a CSD wave to cross the interelectrode distance. Acute and chronic treatment with ethanol, respectively, shortened and increased latencies versus control conditions. Tocopherol treatment counteracted this effect of ethanol.