Sugar consumption induces the consummatory suppression of sugary ethanol: Differential effects of sugar restriction according to sex and age.

Sweet foods activate the reward system that is essential in processing natural reinforcers. Maturation changes in this system during adolescence are linked to heightened impulsivity and risk-seeking behavior, including the use of drugs like ethanol. This usually starts with the consumption of sugary mixtures. However, the influence of sugar exposure on ethanol consumption remains inconclusive. The present research examines the effect of long-term sugar exposure on sugary ethanol (S-EtOH) preference and net intake, exploring the implications of sex, age, accessor restriction of sugar, and its effect during the transition into adulthood. Wistar rats of both sexes were given 24-hour access to a sugar solution for 21 days during adolescence or adulthood. Subsequently, four preference tests of S-EtOH vs. water were carried out every other day, with or without sugar access between each preference test. Our results demonstrate that continuous acute and long-term sugar access induces a consummatory suppression effect on S-EtOH intake, particularly in adult rats, irrespective of sex. This effect becomes more pronounced with more extended periods of exposure to sugar, leading to a higher prevalence of low consumers. Notably, when sugar access was restricted after high familiarization, the suppression effect in adolescent male rats was reduced. Under these conditions, the rats appeared to be more susceptible to developing a preference for S-EtOH consumption. Furthermore, our longitudinal observations reveal that sugar access or restriction conditions during the transition from adolescence to adulthood play a crucial role in shaping S-EtOH consumption patterns in adulthood.

Circadian disruption favors alcohol consumption and differential ΔFosB accumulation in Corticolimbic structures.

Shift-work and exposure to light at night lead to circadian disruption, which favors the use of alcohol and may be a risk factor for development of addictive behavior. This study evaluated in two experimental models of circadian disruption behavioral indicators of elevated alcohol intake and looked for ΔFosB, which is a transcription factor for neuronal plasticity in corticolimbic structures. Male Wistar rats were exposed to experimental shift-work (AR) or to constant light (LL) and were compared with a control group (LD). After 4 weeks in their corresponding conditions, control LD rats remained rhythmic, AR rats exhibited a loss of day-night patterns in the brain and the LL rats showed arrhythmicity in general activity and day-night PER1 patterns in corticolimbic structures. During 12 days of exposure to 10 percent alcohol solution, the AR group showed daily increased alcohol intake while LD and LL rats ingested similar amounts. After 72 h of alcohol deprivation, AR and LL rats increased alcohol intake in a binge-like test; this could be due not only to circadian disruption but also to stress and/or anxiety developed from the AR and LL manipulations. Associated to the increased alcohol intake, the AR and LL rats had significant accumulation of ΔFosB in the nucleus accumbens shell and decreased ΔFosB in the infralimbic cortex. Data here reported confirm that the disruption of temporal patterns favors the increased alcohol consumption and that this is associated with a differential accumulation of ΔFosB which may favor the development of addictive behavior.