ArticleNeuropharmacology2025
Moderate prenatal alcohol exposure alters GABAergic transmission and the actions of acute alcohol in the medial central amygdala of adolescent rats.
Article in Neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed.
- Moderate prenatal alcohol exposure differentially alters acute ethanol sensitivity of GABAergic transmission in CRFR1- and CRFR1+ CeM Neurons.Addiction neuroscience · 2026Article
- Assessment of GABANeuroscience letters · 2026Article
- Age- and sex- dependent effects of moderate gestational day 12 prenatal alcohol exposure on anxiety-like behaviors, ethanol intake, and mechanical sensitivity.bioRxiv : the preprint server for biology · 2026Article
- Anxiety, Depression, and Emotional Dysregulation Following Prenatal Substance Exposure.Advances in experimental medicine and biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Individuals with prenatal alcohol exposure (PAE) are at a higher risk for developing alcohol use disorder (AUD). Using a rat model of moderate PAE (mPAE) on gestational day 12 (G12; ∼2nd trimesters in humans), a critical period for amygdala development, we have shown disruptions in medial central amygdala (CeM) function, an important brain region associated with the development of AUD. In addition to this, acute ethanol (EtOH) increases GABA transmission in the CeM of rodents in a sex-dependent manner, a mechanism that potentially contributes to alcohol misuse. How mPAE alters acute alcohol's effects within the CeM is unknown. Given these findings, we investigated how mPAE may interact with acute alcohol to alter neuronal and synaptic mechanisms in the CeM of adolescent rats in order to understand PAE-induced alcohol-related behaviors. Under basal conditions, mPAE males showed reduced rheobase, indicative of reduced excitability, and females showed a reduction in GABA transmission, indicated by lower spontaneous inhibitory postsynaptic currents (sIPSCs). We found that acute EtOH increased sIPSCs in control males at the middle concentration (66 mM), while mPAE males showed increased sIPSCs only at the highest tested concentration (88 mM). Adolescent females, regardless of PAE status, were largely insensitive to EtOH's effects at all tested concentrations. However, mPAE females showed a significant increase in sIPSCs at the highest tested concentration (88 mM). Overall, these findings support the hypothesis that mPAE leads to sex-specific changes in synaptic activity and neuronal function. Future research is needed to better understand the specific mechanisms by which acute EtOH affects neurotransmission in the adolescent brain of individuals with a history of PAE.
Indexed as
Identifiers
What OpenQuestion holds
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.