Abstract
Binge drinking is common among adolescents, and this type of ethanol exposure may lead to long-term nervous system damage. In the current study, we evaluated motor performance and tissue alterations in the cerebral cortex of rats subjected to intermittent intoxication with ethanol from adolescence to adulthood. Adolescent male Wistar rats (35 days old) were treated with distilled water or ethanol (6.5 g/kg/day, 22.5% w/v) during 55 days by gavage to complete 90 days of age. The open field, inclined plane and the rotarod tests were used to assess the spontaneous locomotor activity and motor coordination performance in adult animals. Following completion of behavioral tests, half of animals were submitted to immunohistochemical evaluation of NeuN (marker of neuronal bodies), GFAP (a marker of astrocytes) and Iba1 (microglia marker) in the cerebral cortex while the other half of the animals were subjected to analysis of oxidative stress markers by biochemical assays. Chronic ethanol intoxication in rats from adolescence to adulthood induced significant motor deficits including impaired spontaneous locomotion, coordination and muscle strength. These behavioral impairments were accompanied by marked changes in all cellular populations evaluated as well as increased levels of nitrite and lipid peroxidation in the cerebral cortex. These findings indicate that continuous ethanol intoxication from adolescence to adulthood is able to provide neurobehavioral and neurodegenerative damage to cerebral cortex.
Highlights
According to World Health Organization (WHO), the abusive consume of ethanol (EtOH) is responsible by over 2.5 million of premature deaths per year and almost 4% of all deaths worldwide are attributed to alcohol
Effects of chronic EtOH exposure during adolescence on body weight gain in rats As illustrated in Fig. 2, the body weight of the animals was evaluated during the entire period (55 days) of ethanol exposure at intervals of
Post-hoc comparisons revealed that ethanol exposure during adolescence induced a significant decrease in the latencies to fall in the four test sessions of the rotarod (Fig. 3C)
Summary
According to World Health Organization (WHO), the abusive consume of ethanol (EtOH) is responsible by over 2.5 million of premature deaths per year and almost 4% of all deaths worldwide are attributed to alcohol. Recent projections have indicated that EtOH consumption will continue to rise in coming decades, and that young adults are at highest increment in rising rates of consumption [1] In this context, the last National Survey on Alcohol and Drug Use in Brazil [2] indicated that alcohol consumption is increasing, mainly among adolescents, becoming a serious health problem. The last National Survey on Alcohol and Drug Use in Brazil [2] indicated that alcohol consumption is increasing, mainly among adolescents, becoming a serious health problem Some brain regions, such as the cerebral cortex, hippocampus and cerebellum, are highly vulnerable to chronic EtOH exposure and significant reduction in brain weight and volume has been found among alcoholics [3,4,5]. The exact molecular mechanisms associated with EtOHinduced brain damage remain to be elucidated, previous studies have demonstrated the role of neuroinflammatory and oxidative stress processes [12,14,16,17]
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