Vitamin B12 administration prevents ethanol-induced learning and memory impairment through re-establishment of the brain oxidant/antioxidant balance, enhancement of BDNF and suppression of GFAP

There are growing evidence indicating that the adolescent brain is persistently affected by the use of psychos-timulant agents. In this regard, alcohol drinking has become rather common among the adolescents in many societies during the last decade. It is currently well known that long-term ethanol exposure deteriorates various cognitive functions such as learning and memory. Mechanistically, these adverse effects have been shown to be mediated by oxidative damage to central nervous system. On the other hand, Vit-B12 is known to improve cognitive performance by suppression of oxidative parameters. Thus, in the present study we aimed to test whether treatment by Vit-B12 could prevent ethanol-induced complications in mice using behavioral and biochemical methods. Different groups of male Syrian mice received ethanol, ethanol+Vit-B12, Vit-B12 alone, or saline during adolescence and then learning and memory functions were assessed by Morris water maze (MWM) and Passive Avoidance (PA) tests. Finally, mice were sacrificed for measurement of biochemical factors. Results indicated that, adolescent ethanol intake impairs learning and memory function through exacerbation of oxidative stress and Vit-B12 treatment improves these complications by re-establishment of oxidant/anti-oxidant balance in CNS. Moreover, we found that Vit-B12 prevents ethanol-induced reduction of BDNF and enhancement of GFAP and acetylcholinesterase (AChE) activity. In conclusion, it seems that Vit-B12 supplementation could be used as an effective therapeutic strategy to prevent learning and memory defects induced by chronic alcohol intake during adolescence.

Automated summary

There is increasing evidence that the adolescent brain is affected by the use of psychostimulant agents, such as alcohol. Long-term alcohol exposure has been found to impair cognitive functions, and this is thought to be mediated by oxidative damage to the central nervous system. However, treatment with Vitamin B12 has been shown to improve cognitive performance by suppressing oxidative parameters. In this study, the researchers aimed to test whether Vitamin B12 treatment could prevent ethanol-induced complications in adolescent mice. The results indicated that adolescent ethanol intake impairs learning and memory function through exacerbation of oxidative stress, but treatment with Vitamin B12 improves these complications by restoring the oxidant/antioxidant balance. Additionally, Vitamin B12 was found to prevent the reduction of BDNF and the enhancement of GFAP and acetylcholinesterase activity induced by ethanol. In conclusion, Vitamin B12 supplementation could be an effective therapeutic strategy to prevent learning and memory defects caused by chronic alcohol intake during adolescence.