Chronic Ethanol Exposure during Adolescence in Rats Induces Motor Impairments and Cerebral Cortex Damage Associated with Oxidative Stress

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.

Chronic ethanol exposure during adolescence through early adulthood in female rats induces emotional and memory deficits associated with morphological and molecular alterations in hippocampus

“…These results corroborate previous findings from our group showing a marked reduction of Iba-1+ cells labeled in the motor cortex of adult male rats following chronic ethanol intoxication during adolescence through early adulthood (Teixeira et al, 2014). On the other hand, we observed that chronic ethanol exposure increased the number of microglial round-shaped cells in the hippocampus.…”

Toxic effect of aflatoxin B1 and the role of recovery on the rat cerebral cortex and hippocampus

“…Previous reports have shown that AFB1 administration reduces total number of cultured glia and neurons (Nones et al, 2012;. The reduction of astrocyte number in the motor cortex was also reported after chronic ethanol exposure and in animal model of streptozotocin-induced diabetes (Coleman et al, 2004;Teixeira et al, 2014). Many evidences indicate the important pathological role of astrocytic dysfunction in several conditions (Cotter et al, 2001).…”

“…However, interestingly, similar effect to that of the CA1 region was only observed after 8 weeks of AFB1 withdrawal in the frontal cortex of the recovery group. This difference in the timing of the AFB1-induced cellular loss in the hippocampus and the frontal cortex might be explained by the fact that the hippocampal cells are more sensitive to AFB1-induced oxidative stress compared to the cortical cells which might require prolonged AFB1 exposure to display neurodegeneration (Teixeira et al, 2014). In contrast to the hippocampus, there was a significant reduction in the astrocyte number in the frontal cortex after AFB1 administration which was rescued after aflatoxin withdrawal.…”

Neurodegeneration and Glial Response after Acute Striatal Stroke: Histological Basis for Neuroprotective Studies

“…Activated microglia/macrophages were labeled using the antibody anti-rat CD68 (clone ED1, 1 : 500, Serotec, UK), which binds to an epitope on the lysosomal membrane of activated macrophages/microglia [38–40], rabbit anti-Iba1 (1 : 1000, WAKO), an antibody that recognizes a calcium binding protein present in the cytoplasm of microglia [41–43], and mouse anti-MHC-II (1 : 100, Serotec), an antibody that recognizes the major histocompatibility complex class II molecule [7]. …”