Abstract
The development of alcohol dependence and depression is determined by various genetic and environmental factors. In the presented study, we used high analgesia (HA) and low analgesia (LA) mouse lines, characterized by different endogenous opioid system activity and divergent blood–brain barrier permeability, to determine the influence of cross-fostering of these lines raised by surrogate mothers on ethanol consumption and development of depressive-like behaviors. We also investigated ethanol drinking by biological parents or surrogate mothers. Furthermore, we investigated whether these parental changes would alter the effect of naloxone on ethanol intake and depressive-like behaviors in offspring. Our results reveal that cross-fostering of HA and LA raised by surrogate mothers has a greater impact on depressive-like behaviors than ethanol consumption. Ethanol intake by biological parents substantially affected depressive-like behaviors and ethanol consumption in offspring. Moreover, ethanol intake by biological parents or an adoptive mother modified the effect of naloxone on ethanol consumption and preference and depressive-like behaviors in the HA offspring only. Together, these results indicate that cross-fostering differentially affects the effect of naloxone on alcohol consumption and the development of depression.
Highlights
Alcohol dependence represents a serious public health problem worldwide
Two-way analysis of variance (ANOVA) taking line and variant as independent factors revealed that ethanol intake did not differ between lines (F(1,89) = 0.076; p = 0.78–line) or variants (F(8,89) = 1.65; p = 0.12–variant)
To summarize, based on our research findings derived from high analgesia (HA) and low analgesia (LA) progeny that were challenged by the interplay of several inherent and environmental factors—such as the genetic predisposition to depression, different ethanol use background of biological or surrogate parents, rearing by a foster caregiver, and treatment with an opioid antagonist— we have demonstrated that some external influences experienced postnatally, such as susceptibility to alcohol use disorders (AUD), can be transmitted epigenetically from parents to generations
Summary
Alcohol dependence represents a serious public health problem worldwide. Major public health and social hazards of alcoholism include cognitive decline [1], weakened social and familial connections [2], rise in crime and related issues or social status, losses, and a decrease in professional productivity [3]. Social separation increases ethanol intake and preference in mice as well [7] Other societal factors, such as forced endurance of a crowded place or domination/submission-like interactions between individuals in a group, elicit ethanol overuse [7]. A hostile societal environment or individual inherent deficits place subjects at risk of social relationship deprivation and generate motor overactivity and anxiety or depression in rodents [8]. These changes are likely mediated by serotonergic signaling decline or alterations in the functioning of the mesolimbic dopaminergic pathway [9]
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