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Pairing a conditioned stimulus (CS) with ethanol generally produces aversion for that CS in adult rodents. However, infant rats (PD1-PD3) exposed to ethanol demonstrate appetitive reinforcement to ethanol (Nizhnikov, Varlinskaya, Petrov, & Spear, 2006; Petrov, Varlinskaya, & Spear, 2003). This sensitivity to the appetitive properties of ethanol during infancy may be transient, as during the second postnatal week rat pups tend to exhibit conditioned aversions to flavors paired with ethanol. The present study examined changes in the motivation properties of ethanol through ontogeny and the neurobiology underlying these changes. Rat pups were exposed to a taste conditioning procedure on PD4 or PD12. Rat pups were intraorally infused with 2.5% of their body weight of saccharin solution (0.1%) and immediately after injected intraperitoneolly (i.p.) with one of six doses of ethanol (0.0-2.0 g/kg). A day later pups were given saccharine infusions and percent body weight gain was used as an index of ethanol's reinforcing effects. PD4 pups expressed appetitive reinforcement to ethanol, as indicated by greater saccharin intake, as compared to control counterparts and to the older PD12 pups. Subsequent experiments revealed that PD4 pups were less sensitive to the aversive properties of the drug than PD12 pups. The older pups found high doses of ethanol aversive while PD4 rat pups did not condition aversions to this dose of ethanol after a single trial. A similar pattern of results was observed between the low doses of ethanol and the highest doses of a kappa opioid agonist. The PD12 animals did not condition to the kappa opioid agonist, while the younger rats expressed an appetitive response. These results illustrate an ontogenetic change in the motivational properties of ethanol, with sensitivity to its appetitive properties declining and responsiveness to the aversive properties increasing with age during early infancy.

Pairing a conditioned stimulus (CS) with ethanol generally produces aversion for that CS in adult rodents. However, infant rats (PD1-PD3) exposed to ethanol demonstrate appetitive reinforcement to ethanol (Nizhnikov, Varlinskaya, Petrov, & Spear, 2006; Petrov, Varlinskaya, & Spear, 2003). This sensitivity to the appetitive properties of ethanol during infancy may be transient, as during the second postnatal week rat pups tend to exhibit conditioned aversions to flavors paired with ethanol. The present study examined changes in the motivation properties of ethanol through ontogeny and the neurobiology underlying these changes. Rat pups were exposed to a taste conditioning procedure on PD4 or PD12. Rat pups were intraorally infused with 2.5% of their body weight of saccharin solution (0.1%) and immediately after injected intraperitoneolly (i.p.) with one of six doses of ethanol (0.0-2.0 g/kg). A day later pups were given saccharine infusions and percent body weight gain was used as an index of ethanol's reinforcing effects. PD4 pups expressed appetitive reinforcement to ethanol, as indicated by greater saccharin intake, as compared to control counterparts and to the older PD12 pups. Subsequent experiments revealed that PD4 pups were less sensitive to the aversive properties of the drug than PD12 pups. The older pups found high doses of ethanol aversive while PD4 rat pups did not condition aversions to this dose of ethanol after a single trial. A similar pattern of results was observed between the low doses of ethanol and the highest doses of a kappa opioid agonist. The PD12 animals did not condition to the kappa opioid agonist, while the younger rats expressed an appetitive response. These results illustrate an ontogenetic change in the motivational properties of ethanol, with sensitivity to its appetitive properties declining and responsiveness to the aversive properties increasing with age during early infancy.

Alcohol use, binge drinking, and alcohol use disorders have been increasing among older adults in the US population, including adults over 50 as well as adults over 65. Increases in consumption are sharper among women, and among those who use additional substances such as cannabis, and those who are relatively healthy in older adulthood (i.e. those without multimorbidites). This commentary describes these trends as well as provides hypotheses, and the data underlying them, for both supply-side (alcohol marketing and messaging) and demand-side (healthier aging, increased financial stress) potential drivers of these increases. The need for additional resources and focus on older adult drinking is increasingly urgent, as alcohol-attributable deaths escalate among older adults in the United States.

Alcohol use, binge drinking, and alcohol use disorders have been increasing among older adults in the US population, including adults over 50 as well as adults over 65. Increases in consumption are sharper among women, and among those who use additional substances such as cannabis, and those who are relatively healthy in older adulthood (i.e. those without multimorbidites). This commentary describes these trends as well as provides hypotheses, and the data underlying them, for both supply-side (alcohol marketing and messaging) and demand-side (healthier aging, increased financial stress) potential drivers of these increases. The need for additional resources and focus on older adult drinking is increasingly urgent, as alcohol-attributable deaths escalate among older adults in the United States.

Science is now in a new era of exposome research that strives to build a more all-inclusive, panoramic view in the quest for answers; this is especially true in the field of toxicology. Alcohol exposure researchers have been examining the multivariate co-exposures that may either exacerbate or initiate alcohol-related tissue/organ injuries. This manuscript presents selected key variables that represent the Alcohol Exposome. The primary variables that make up the Alcohol Exposome can include comorbidities such as cigarettes, poor diet, occupational hazards, environmental hazards, infectious agents, and aging. In addition to representing multiple factors, the Alcohol Exposome examines the various types of intercellular communications that are carried from one organ system to another and may greatly impact the types of injuries and metabolites caused by alcohol exposure. The intent of defining the Alcohol Exposome is to bring the newly expanded definition of Exposomics, meaning the study of the exposome, to the field of alcohol research and to emphasize the need for examining research results in a non-isolated environment representing a more relevant manner in which all human physiology exists.

Science is now in a new era of exposome research that strives to build a more all-inclusive, panoramic view in the quest for answers; this is especially true in the field of toxicology. Alcohol exposure researchers have been examining the multivariate co-exposures that may either exacerbate or initiate alcohol-related tissue/organ injuries. This manuscript presents selected key variables that represent the Alcohol Exposome. The primary variables that make up the Alcohol Exposome can include comorbidities such as cigarettes, poor diet, occupational hazards, environmental hazards, infectious agents, and aging. In addition to representing multiple factors, the Alcohol Exposome examines the various types of intercellular communications that are carried from one organ system to another and may greatly impact the types of injuries and metabolites caused by alcohol exposure. The intent of defining the Alcohol Exposome is to bring the newly expanded definition of Exposomics, meaning the study of the exposome, to the field of alcohol research and to emphasize the need for examining research results in a non-isolated environment representing a more relevant manner in which all human physiology exists.

Decreases in birth weight are among the most commonly reported effects of prenatal alcohol exposure in animals. However, these decreases are typically associated with relatively high doses of alcohol. Two studies were conducted. The first evaluated the effects of low doses of alcohol (0.15 and 0.30 g/kg) on birth weight and other measures. A second study examined the effects of a relatively high dose of alcohol (3.0 g/kg). The two low doses of alcohol produced a slight, but not significant, increase in birth weight relative to vehicle controls whereas the high dose of alcohol produced a significant decrease in birth weight relative to its controls. When the data for the two studies were combined, the relationship between alcohol and birth weight assumed an inverted U-shaped function. There was no effect of prenatal alcohol exposure on weights at weaning, passive avoidance learning, or ambulation. In the context of birth weight, slight increases may be related to increased protein synthesis associated with low doses of alcohol.

Decreases in birth weight are among the most commonly reported effects of prenatal alcohol exposure in animals. However, these decreases are typically associated with relatively high doses of alcohol. Two studies were conducted. The first evaluated the effects of low doses of alcohol (0.15 and 0.30 g/kg) on birth weight and other measures. A second study examined the effects of a relatively high dose of alcohol (3.0 g/kg). The two low doses of alcohol produced a slight, but not significant, increase in birth weight relative to vehicle controls whereas the high dose of alcohol produced a significant decrease in birth weight relative to its controls. When the data for the two studies were combined, the relationship between alcohol and birth weight assumed an inverted U-shaped function. There was no effect of prenatal alcohol exposure on weights at weaning, passive avoidance learning, or ambulation. In the context of birth weight, slight increases may be related to increased protein synthesis associated with low doses of alcohol.