ArticleBehavioural brain research2019
Prenatal ethanol exposure increases risk of psychostimulant addiction.
Article in Behavioural brain research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Environmental enrichment reverses prenatal ethanol exposure-induced attention-deficits in rats.Frontiers in psychiatry · 2025Article
- Developmental alcohol exposure is exhausting: Sleep and the enduring consequences of alcohol exposure during development.Neuroscience and biobehavioral reviews · 2024Review
- Embryonic ethanol exposure and optogenetic activation of hypocretin neurons stimulate similar behaviors early in life associated with later alcohol consumption.Scientific reports · 2024Article
- Review
- Combined exposure to alcohol and cannabis during development: Mechanisms and outcomes.Alcohol (Fayetteville, N.Y.) · 2023Review
- Prenatal ethanol exposure leads to persistent anxiety-like behavior during adulthood indicated by reduced horizontal and vertical exploratory behaviors.Frontiers in neuroscience · 2023Article
- Prenatal ethanol exposure impairs sensory processing and habituation to visual stimuli, effects normalized by enrichment of postnatal environmental.Alcoholism, clinical and experimental research · 2022Article
- DNA Epigenetics in Addiction Susceptibility.Frontiers in genetics · 2022Review
- Combined and sequential effects of alcohol and methamphetamine in animal models.Neuroscience and biobehavioral reviews · 2021Review
- Moderate prenatal ethanol exposure leads to attention deficits in both male and female rats.Alcoholism, clinical and experimental research · 2021Article
- Prenatal opioid exposure and vulnerability to future substance use disorders in offspring.Experimental neurology · 2021Review
- Article
- Prenatal Alcohol Exposure in Rats Diminishes Postnatal Cxcl16 Chemokine Ligand Brain Expression.Brain sciences · 2020Article
- Cocaine self-administration abolishes endocannabinoid-mediated long-term depression of glutamatergic synapses in the ventral tegmental area.The European journal of neuroscience · 2020Article
- Prenatal and postnatal alcohol exposure increases vulnerability to cocaine addiction in adult mice.British journal of pharmacology · 2020Article
- The Transgenerational Consequences of the Interaction Between Humans and Molecules: Alcohol as a Cultural Artifact.Frontiers in psychology · 2020Article
- Prenatal Ethanol Exposure Leads to Attention Deficits in Both Male and Female Rats.Frontiers in neuroscience · 2020Article
- Review
- Environmental enrichment reverses increased addiction risk caused by prenatal ethanol exposure.Drug and alcohol dependence · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Prenatal ethanol exposure (PE) causes many cognitive and behavioral deficits including increased drug addiction risk, demonstrated by enhanced ethanol intake and behavioral phenotypes associated with addiction risk. Additionally, preclinical studies show that PE persistently changes the function of dopaminergic neurons in the ventral tegmental area, a major neural substrate for addiction, and alters these neurons' responses to psychostimulants. Accordingly, PE could also lead to increased risk of addiction to drugs of abuse, other than ethanol. In the present study, addiction risk was examined utilizing paradigms of amphetamine conditioned place preference (CPP) and intravenous self-administration. Ethanol was administered to pregnant dams via intragastric gavage (6 g/kg, during gestational days 8-20). Behavioral tests were conducted in adult male offspring. Amphetamine at a low dose (0.3 mg/kg, i.p.) induced CPP in PE but not control rats, whereas at a higher dose (0.6 mg/kg, i.p.) both groups acquired CPP. There was no group difference in amphetamine-induced CPP reinstatement. Furthermore, PE rats self-administered more amphetamine at a low dose (0.02 mg/kg/infusion) than controls, while no group differences were observed at a higher dose (0.1 mg/kg/infusion). Rats with PE also exhibited greater reactivity to contextual drug cues after extended abstinence and amphetamine-induced reinstatement of drug seeking. These results support that PE persistently leads to increased psychostimulant addiction risk later in life, manifested in many elements of addictive behavior following limited psychostimulant exposure. The observations provide insights into prevention strategies for drug addiction in individuals with fetal alcohol spectrum disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.