• Acute Ethanol;
  • Astaxanthin;
  • Antioxidants;
  • Spreading depression


Ethanol (EtOH) abuse and insufficient ingestion of antioxidants are external factors that can alter brain electrophysiology. Our previous studies have demonstrated that the excitability-related brain electrophysiological phenomenon known as cortical spreading depression (CSD) was facilitated by chronic EtOH intake, and chronic treatment with carotenoids attenuated this effect. Here, we investigated the acute effect of a single EtOH administration on CSD in young and adult rats previously (1 hour) treated with 10 μg/kg of astaxanthin.


Male Wistar rats (5 young- and 5 adult groups, 60 to 80 and 150 to 180 days of age, respectively) were treated by 2 gavage procedures at 1-hour interval as follows: groups 1 and 2 received astaxanthin in gavage I combined with EtOH (group 1) or water (group 2) in gavage II; groups 3 and 4 received olive oil (the vehicle in which astaxanthin was dissolved) in gavage I combined with EtOH (group 3) or water (group 4) in gavage II; group 5 received water in gavage I combined with EtOH in gavage II. CSD was recorded on the cortical surface for 4 hours.


Compared to the respective water and oil controls (groups 2 and 4; CSD velocities: 3.73 ± 0.09 and 3.78 ± 0.07 mm/min in the young groups; 2.99 ± 0.10 and 3.05 ± 0.19 mm/min in the adult groups), a single dose of EtOH (groups 3 and 5) decreased CSD propagation velocities (3.29 ± 0.23 and 3.16 ± 0.10 mm/min in the young groups; 2.71 ± 0.27 and 2.75 ± 0.31 mm/min in the adult groups). Astaxanthin antagonized the impairing effect of acute EtOH on CSD (group 1; mean velocity: 3.70 ± 0.19 and 3.13 ± 0.16 mm/min for the young and adult groups, respectively).


The results showed an antagonistic effect of acute EtOH treatment on CSD propagation that was reverted by astaxanthin. The EtOH–astaxanthin interaction was not influenced by the age, as it was found in both young and adult animals.