Abstract:Ethanol abuse is linked to several acute and chronic injuries that can lead to health
problems. Ethanol addiction is one of the most severe diseases linked to the abuse of
this drug. Symptoms of ethanol addiction include compulsive substance intake and
withdrawal syndrome. Stress exposure has an important role in addictive behavior for
many drugs of abuse (including ethanol), but the consequences of stress and ethanol
in the organism when these factors are concomitant results in a complex interaction.
We inves… Show more
“…Twenty-four hours after the last ethanol binge, basal anxiety in the light–dark apparatus was similar between ethanol-exposed and control mice. Others have reported withdrawal-induced anxiety in adolescent rats ( Pandey et al, 2015 ; Kyzar et al, 2016 ), although this is not consistently found ( Kiefer et al, 2003 ; Lee et al, 2016 ; Morais-Silva et al, 2016 ). Indeed, some have suggested that adolescent mice are resilient to early ethanol withdrawal ( Lee et al, 2016 ) and it is possible that binge ethanol in adolescence only produces lasting withdrawal-induced anxiety in rats and not mice.…”
Adolescents primarily consume alcohol in binges, which can be particularly harmful to the developing frontal cortex and increase risk for an adult alcohol use disorder. We conducted a study investigating immediate and long lasting changes to the prefrontal cortex (PFC) transcriptome to determine the molecular mechanisms underlying adult ethanol behavioral sensitivity following binge ethanol in adolescence. DBA/2J mice were orally dosed with 4 g/kg ethanol intermittently from day 29 to 42. Adolescent mice were tested for anxiety-like behavior and ethanol sensitivity using the loss of righting reflex task. As adults, mice were tested for cognitive changes using the novel object recognition task, ethanol-induced anxiolysis and ethanol sensitivity. Adolescent binge ethanol altered ethanol sensitivity in young mice and led to lasting memory deficits in the object recognition test and greater ethanol sensitivity in adulthood. Using genomic profiling of transcripts in the PFC, we found that binge ethanol reduced myelin-related gene expression and altered chromatin modifying genes involved in histone demethylation at H3K9 and H3K36. We hypothesize that ethanol’s actions on histone methylation may be a switch for future transcriptional changes that underlie the behavioral changes lasting into adulthood.
“…Twenty-four hours after the last ethanol binge, basal anxiety in the light–dark apparatus was similar between ethanol-exposed and control mice. Others have reported withdrawal-induced anxiety in adolescent rats ( Pandey et al, 2015 ; Kyzar et al, 2016 ), although this is not consistently found ( Kiefer et al, 2003 ; Lee et al, 2016 ; Morais-Silva et al, 2016 ). Indeed, some have suggested that adolescent mice are resilient to early ethanol withdrawal ( Lee et al, 2016 ) and it is possible that binge ethanol in adolescence only produces lasting withdrawal-induced anxiety in rats and not mice.…”
Adolescents primarily consume alcohol in binges, which can be particularly harmful to the developing frontal cortex and increase risk for an adult alcohol use disorder. We conducted a study investigating immediate and long lasting changes to the prefrontal cortex (PFC) transcriptome to determine the molecular mechanisms underlying adult ethanol behavioral sensitivity following binge ethanol in adolescence. DBA/2J mice were orally dosed with 4 g/kg ethanol intermittently from day 29 to 42. Adolescent mice were tested for anxiety-like behavior and ethanol sensitivity using the loss of righting reflex task. As adults, mice were tested for cognitive changes using the novel object recognition task, ethanol-induced anxiolysis and ethanol sensitivity. Adolescent binge ethanol altered ethanol sensitivity in young mice and led to lasting memory deficits in the object recognition test and greater ethanol sensitivity in adulthood. Using genomic profiling of transcripts in the PFC, we found that binge ethanol reduced myelin-related gene expression and altered chromatin modifying genes involved in histone demethylation at H3K9 and H3K36. We hypothesize that ethanol’s actions on histone methylation may be a switch for future transcriptional changes that underlie the behavioral changes lasting into adulthood.
“…Mice were individually placed in the middle of the arena and were allowed to explore freely the apparatus for 5 min. Analysis included measures of the distance travelled in central (central locomotion) and peripheral area (peripheral locomotion), as well as the total distance travelled (i.e., center + periphery) (total locomotion) [ 32 , 33 ].…”
Section: Methodsmentioning
confidence: 99%
“…Ten min later, the object A’ was replaced by a rectangular object B, and the short-term memory was assessed. The long-term memory was evaluated 24 h later in the same apparatus by changing the object B by a new object, an orange sphere called object C. The same animals were evaluated for short- and long-term memory [ 32 , 33 ].…”
Section: Methodsmentioning
confidence: 99%
“…For each object, the interaction period was defined as the time while the animal remained in physical contact with the object. Data were presented as the discrimination index, which was determined by time spent on the new object divided by the time spent on both objects [ 32 , 33 ].…”
The aim of this study was to investigate the effect of rosuvastatin treatment on memory impairment, and anxiogenic-like effects in mice chronically infected with Toxoplasma gondii. For this, Balb/c mice were infected orally with chronic ME-49 strain of Toxoplasma gondii. Oral treatment with rosuvastatin (40mg/kg/day) started on the 51st day post-infection and was performed daily for 21 days. After completion of treatment, anxiety-like effects and locomotion were investigated in the open field (OF) test, whereas novel object recognition (NOR) test was used for evaluation of short- and long-term memory. At the end of the experiments, the brain was collected for Toxoplasma gondii DNA quantification and histopathological analysis. Infection with ME-49 strain decreased the time spent in the center of OF, indicating an anxiogenic effect, without affecting total and peripheral locomotion. Rosuvastatin treatment inhibited the change in the center time. Besides, pharmacological treatment increased total and central locomotion in both non-infected and infected animals. Infection also impaired both short- and long-term memory in the NOR test, and these effects were reverted by rosuvastatin treatment. In addition to effects in behavioral changes, rosuvastatin also reduced parasite load in the brain and attenuated signs of brain inflammation such as perivascular cuffs, inflammatory cell infiltration and tissue damage. These findings indicate for the first time the efficacy of rosuvastatin in treatment of memory impairment and anxiogenic effect evoked by infection with Toxoplasma gondii. These effects might be mediated by reduced cyst load, which in turn decrease inflammation and damage in the brain.
“…Indeed, behavioral crosssensitization is observed between stress and ethanol in both adolescent and adult rodents (for review, see Burke & Miczek, 2014). Stress exposure can raise ethanol intake and preference in both animals (Morais-Silva, Fernandes-Santos, Moreira-Silva, & Marin, 2016;Norman et al, 2015;Quadir et al, 2016) and humans (Sinha, 2001), although some studies have shown no impact of stress or a reduction in ethanol intake when rodents have access to alcohol during or immediately after stress (van Erp & Miczek, 2001;Marianno, Abrahao, & Camarini, 2017). Stress exposure also increases behavioral sensitivity to ethanol (Quadir et al, 2016).…”
a b s t r a c tThe peculiar neurochemical profile of the adolescent brain renders it differently susceptible to several stimuli, including stress and/or drug exposure. Among several stress mediators, nitric oxide (NO) has a role in stress responses. We have demonstrated that adolescent mice are less sensitive to ethanolinduced sensitization than adult mice. The present study investigated whether chronic unpredictable stress (CUS) induces behavioral sensitization to ethanol in adolescent and adult Swiss mice, and investigated the influence of Ca 2þ -dependent nitric oxide synthase (NOS) activity in the phenomenon.Adolescent and adult mice were exposed to repeated 1.8 g/kg ethanol or CUS and challenged with saline or ethanol. A neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7NI), was administered along with ethanol and CUS to test its effects on behavioral sensitization. Both adolescent and adult mice displayed cross-sensitization between CUS and ethanol in adult mice, with adolescents showing a lower degree of sensitization than adults. nNOS inhibition by 7NI reduced both ethanol sensitization and crosssensitization. All age differences in the Ca 2þ -dependent NOS activity in the hippocampus and prefrontal cortex were in the direction of greater activity in adults than in adolescents. Adolescents showed lower sensitivity to cross-sensitization between CUS and ethanol, and the nitric oxide (NO) system seems to have a pivotal role in ethanol-induced behavioral sensitization and cross-sensitization in both adolescent and adult mice.
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