Prenatal Alcohol Exposure as a Case of Involuntary Early Onset of Alcohol Use: Consequences and Proposed Mechanisms From Animal Studies

Gaztañaga, Mirari; Angulo-Alcalde, Asier; Chotro, M. Gabriela

doi:10.3389/fnbeh.2020.00026

Cited by 11 publications

(9 citation statements)

References 132 publications

(156 reference statements)

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“…Considerable work has been done to study the effects of prenatal alcohol, cocaine, and nicotine exposure. Prenatal alcohol exposure also increases alcohol consumption and alcohol preference in rodents with alterations in the endogenous opioid system hypothesized to underlie the alcohol intake ( Fabio et al, 2015 ; Gaztañaga et al, 2020 ). Epidemiological data also supports the relationship between prenatal alcohol exposure and future risk for alcohol use disorders in humans ( Alati et al, 2006 ).…”

Section: Discussionmentioning

confidence: 99%

Prenatal Opioid Exposure Enhances Responsiveness to Future Drug Reward and Alters Sensitivity to Pain: A Review of Preclinical Models and Contributing Mechanisms

Grecco

Atwood

2020

eNeuro

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The opioid crisis has resulted in an unprecedented number of neonates born with prenatal opioid exposure (POE); however, the long-term effects of POE on offspring behavior and neurodevelopment remain relatively unknown. The advantages and disadvantages of the various preclinical POE models developed over the last several decades are discussed in the context of clinical and translational relevance. Although considerable and important variability exists among preclinical models of POE, the examination of these preclinical models has revealed that opioid exposure during the prenatal period contributes to maladaptive behavioral development as offspring mature including an altered responsiveness to rewarding drugs and increased pain response. The present review summarizes key findings demonstrating the impact of POE on offspring drug selfadministration, drug consumption, the reinforcing properties of drugs, drug tolerance, and other reward-related behaviors such as hypersensitivity to pain. Potential underlying molecular mechanisms which may contribute this enhanced addictive phenotype in POE offspring are further discussed with special attention given to key brain regions associated with reward including the striatum, prefrontal cortex, ventral tegmental area, hippocampus, and amygdala. Improvements in preclinical models and further areas of study are also identified which may advance the translational value of findings and help address the growing problem of POE in clinical populations. Significance Statement As the number of the infants born following prenatal opioid exposure continues to increase, there is a greater need to employ preclinical models to study the potential consequences of POE and brain and behavioral development. A large body of evidence indicates POE is associated with alterations in reward-related behavior and molecular adaptations in reward neurocircuitry. This review seeks to: (1) provide an overview of the various types of preclinical models developed over the last few decades; (2) review the numerous behavioral studies examining drug-reward related behavior in offspring with POE; and (3) discuss potential contributing molecular mechanisms to this enhanced reward phenotype observed in POE offspring.

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Section: Discussionmentioning

confidence: 99%

Prenatal Opioid Exposure Enhances Responsiveness to Future Drug Reward and Alters Sensitivity to Pain: A Review of Preclinical Models and Contributing Mechanisms

Grecco

Atwood

2020

eNeuro

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“…In addition, studies of adopted‐out children of alcoholic mothers confirmed this assertion (Yates, Cadoret, Troughton, Stewart, & Giunta, 1998). Several animal studies support and explain the developmental origins of adolescent alcohol use in humans (Gaztañaga et al, 2020). Animal studies have shown that the effect of PAE transcends beyond the first generation.…”

Section: Developmental Origins Of Adolescent Drinkingmentioning

confidence: 97%

“…However, other studies have shown that this effect does not last beyond early postnatal life (Fabio et al, 2015). The fetus develops an appetitive conditional response to alcohol such that it forms an association between the flavor and its pharmacological effects (Bordner & Deak, 2015; Gaztañaga et al, 2020). In the brain, AA, a metabolite produced from the detoxification of alcohol mediates the production of appetitive properties of alcohol as well as serves as its reinforcing agent by acting on the opioid system (Gaztañaga, Angulo‐Alcalde, Spear, & Chotro, 2017).…”

Section: Prenatal Alcohol Consumption: Mechanisms To Aldmentioning

confidence: 99%

“…For example, the offspring of alcoholic mothers tend to crave and drink alcohol in later life. PAE causes a desire to drink alcohol in adolescence due to appetitive learning induced by the sensory and reinforcing pharmacological properties of alcohol (Gaztañaga et al, 2020). Notably, research reveals that, for every gram of alcohol consumed during adolescence, there is a 2% risk of developing severe liver disease (Hagström, Hemmingsson, Discacciati, & Andreasson, 2018).…”

Section: Introductionmentioning

confidence: 99%

“…Patients with brain abnormalities associated with FASD have been the primary focus of research; meanwhile, other body organs and systems may be affected (Caputo et al, 2016). Parental alcohol exposure (PAE) can program adverse metabolic (Amos-Kroohs et al, 2016;Castells, Mark, Abaci, & Schwartz, 1981) and neurological (Foltran, Gregori, Franchin, Verduci, & Giovannini, 2011;Gaztañaga, Angulo-Alcalde, & Chotro, 2020;Gibson & Porter, 2018) health outcomes in offspring.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Early‐lifeexposure to alcohol and the risk ofalcohol‐inducedliver disease in adulthood

Asiedu

Nyakudya

Lembede

et al. 2021

Birth Defects Research

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Alcohol consumption remains prevalent among pregnant and nursing mothers despite the well‐documented adverse effects this may have on the offspring. Moderate‐to‐high levels of alcohol consumption in pregnancy result in fetal alcohol syndrome (FAS) disorders, with brain defects being chief among the abnormalities. Recent findings indicate that while light‐to‐moderate levels may not cause FAS, it may contribute to epigenetic changes that make the offspring prone to adverse health outcomes including metabolic disorders and an increased propensity in the adolescent‐onset of drinking alcohol. On the one hand, prenatal alcohol exposure (PAE) causes epigenetic changes that affect lipid and glucose transcript regulating genes resulting in metabolic abnormalities. On the other hand, it can program offspring for increased alcohol intake, enhance its palatability, and increase acceptance of alcohol's flavor through associative learning, making alcohol a plausible second hit for the development of alcohol‐induced liver disease. Adolescent drinking results in alcohol dependence and abuse in adulthood. Adolescent drinking results in alcohol dependence and abuse in adulthood. Alterations on the opioid system, particularly, the mu‐opioid system, has been implicated in the mechanism that induces increased alcohol consumption and acceptance. This review proposes a mechanism that links PAE to the development of alcoholism and eventually to alcoholic liver disease (ALD), which results from prolonged alcohol consumption. While PAE may not lead to ALD development in childhood, there are chances that it may lead to ALD in adulthood.

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Classical Conditioning

Hermann

Sperl

2023

Handbook of Clinical Child Psychology

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Prenatal Alcohol Exposure as a Case of Involuntary Early Onset of Alcohol Use: Consequences and Proposed Mechanisms From Animal Studies

Cited by 11 publications

References 132 publications

Prenatal Opioid Exposure Enhances Responsiveness to Future Drug Reward and Alters Sensitivity to Pain: A Review of Preclinical Models and Contributing Mechanisms

Prenatal Opioid Exposure Enhances Responsiveness to Future Drug Reward and Alters Sensitivity to Pain: A Review of Preclinical Models and Contributing Mechanisms

Early‐lifeexposure to alcohol and the risk ofalcohol‐inducedliver disease in adulthood

Classical Conditioning

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