ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Prenatal Ethanol Exposure Persistently Alters Endocannabinoid Signaling and Endocannabinoid-Mediated Excitatory Synaptic Plasticity in Ventral Tegmental Area Dopamine Neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Developmental Neurotoxicity of Alcohol from Neuronal Basis to Behavioural Outcomes: A Comprehensive Review.Neurology international · 2026Review
- Chemogenetic inhibition of prefrontal cortex inputs to dorsal raphe reduces anxiety behaviors in male rat model of fetal alcohol spectrum disorder.Scientific reports · 2025Article
- Prenatal exposure to alcohol and its impact on reward processing and substance use in adulthood.Translational psychiatry · 2024Article
- The role of PPAR-γ in memory deficits induced by prenatal and lactation alcohol exposure in mice.Molecular psychiatry · 2023Article
- Combined exposure to alcohol and cannabis during development: Mechanisms and outcomes.Alcohol (Fayetteville, N.Y.) · 2023Review
- Alcohol & cannabinoid co-use: Implications for impaired fetal brain development following gestational exposure.Experimental neurology · 2023Review
- Review
- Prenatal alcohol exposure dysregulates spinal and circulating immune cell circular RNA expression in adult female rats with chronic sciatic neuropathy.Frontiers in neuroscience · 2023Article
- Endocannabinoids at the synapse and beyond: implications for neuropsychiatric disease pathophysiology and treatment.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Review
- Prenatal ethanol exposure causes anxiety-like phenotype and alters synaptic nitric oxide and endocannabinoid signaling in dorsal raphe nucleus of adult male rats.Translational psychiatry · 2022Article
- Prenatal ethanol exposure impairs sensory processing and habituation to visual stimuli, effects normalized by enrichment of postnatal environmental.Alcoholism, clinical and experimental research · 2022Article
- Moderate prenatal ethanol exposure leads to attention deficits in both male and female rats.Alcoholism, clinical and experimental research · 2021Article
- Prenatal alcohol exposure reduces posterior dorsomedial striatum excitability and motivation in a sex- and age-dependent fashion.Neuropharmacology · 2020Article
- Cocaine self-administration abolishes endocannabinoid-mediated long-term depression of glutamatergic synapses in the ventral tegmental area.The European journal of neuroscience · 2020Article
- Gestational alcohol exposure disrupts cognitive function and striatal circuits in adult offspring.Nature communications · 2020Article
- Distinct functions of endogenous cannabinoid system in alcohol abuse disorders.British journal of pharmacology · 2019Review
- Collateral Projections from the Lateral Parabrachial Nucleus to the Central Amygdaloid Nucleus and the Ventral Tegmental Area in the Rat.Anatomical record (Hoboken, N.J. : 2007) · 2019Article
- Prenatal ethanol exposure increases risk of psychostimulant addiction.Behavioural brain research · 2019Article
- Environmental enrichment reverses increased addiction risk caused by prenatal ethanol exposure.Drug and alcohol dependence · 2018Article
- Persistent effects of obesity: a neuroplasticity hypothesis.Annals of the New York Academy of Sciences · 2018Review
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5 authors at 2 institutions in 1 country.
Funding
Abstract
Prenatal ethanol exposure (PE) leads to increased addiction risk which could be mediated by enhanced excitatory synaptic strength in ventral tegmental area (VTA) dopamine (DA) neurons. Previous studies have shown that PE enhances excitatory synaptic strength by facilitating an anti-Hebbian form of long-term potentiation (LTP). In this study, we investigated the effect of PE on endocannabinoid-mediated long-term depression (eCB-LTD) in VTA DA neurons. Rats were exposed to moderate (3 g/kg/d) or high (6 g/kg/d) levels of ethanol during gestation. Whole-cell recordings were conducted in male offspring between 4 and 10 weeks old.We found that PE led to increased amphetamine self-administration. Both moderate and high levels of PE persistently reduced low-frequency stimulation-induced eCB-LTD. Furthermore, action potential-independent glutamate release was regulated by tonic eCB signaling in PE animals. Mechanistic studies for impaired eCB-LTD revealed that PE downregulated CB1 receptor function. Interestingly, eCB-LTD in PE animals was rescued by metabotropic glutamate receptor I activation, suggesting that PE did not impair the synthesis/release of eCBs. In contrast, eCB-LTD in PE animals was not rescued by increasing presynaptic activity, which actually led to LTP in PE animals, whereas LTD was still observed in controls. This result shows that the regulation of excitatory synaptic plasticity is fundamentally altered in PE animals. Together, PE leads to impaired eCB-LTD at the excitatory synapses of VTA DA neurons primarily due to CB1 receptor downregulation. This effect could contribute to enhanced LTP and the maintenance of augmented excitatory synaptic strength in VTA DA neurons and increased addiction risk after PE.
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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.