ArticleNeuroscience2020
Single-day Postnatal Alcohol Exposure Induces Apoptotic Cell Death and Causes long-term Neuron Loss in Rodent Thalamic Nucleus Reuniens.
Article in Neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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
13 citing papers in PubMed.
- Article
- Choice Behaviors and Prefrontal-Hippocampal Coupling Are Disrupted in a Rat Model of Fetal Alcohol Spectrum Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Impact of Developmental Alcohol Exposure on the Thalamus.Advances in experimental medicine and biology · 2025Review
- Deliberative Behaviors and Prefrontal-Hippocampal Coupling are Disrupted in a Rat Model of Fetal Alcohol Spectrum Disorders.bioRxiv : the preprint server for biology · 2024Article
- Upregulation of mesencephalic astrocyte-derived neurotrophic factor (MANF) expression offers protection against alcohol neurotoxicity.Journal of neurochemistry · 2023Article
- Longitudinal Evaluation Using Preclinical 7T-Magnetic Resonance Imaging/Spectroscopy on Prenatally Dose-Dependent Alcohol-Exposed Rats.Metabolites · 2023Article
- Rat Model of Late Gestational Alcohol Exposure Produces Similar Life-Long Changes in Thalamic Nucleus Reuniens Following Moderate- Versus High-Dose Insult.Alcohol and alcoholism (Oxford, Oxfordshire) · 2022Article
- Potential Role of MANF, an ER Stress Responsive Neurotrophic Factor, in Protecting Against Alcohol Neurotoxicity.Molecular neurobiology · 2022Review
- The nucleus reuniens orchestrates prefrontal-hippocampal synchrony during spatial working memory.Neuroscience and biobehavioral reviews · 2021Review
- Midline Thalamic Damage Associated with Alcohol-Use Disorders: Disruption of Distinct Thalamocortical Pathways and Function.Neuropsychology review · 2021Review
- Executive functioning-specific behavioral impairments in a rat model of human third trimester binge drinking implicate prefrontal-thalamo-hippocampal circuitry in Fetal Alcohol Spectrum Disorders.Behavioural brain research · 2021Article
- Changes in Representation of Thalamic Projection Neurons within Prefrontal-Thalamic-Hippocampal Circuitry in a Rat Model of Third Trimester Binge Drinking.Brain sciences · 2021Article
- Postnatal alcohol exposure and adolescent exercise have opposite effects on cerebellar microglia in rat.International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Fetal alcohol spectrum disorders (FASD) constitute a prevalent, yet preventable, developmental disorder worldwide. While a wealth of research demonstrates that altered function of hippocampus (HPC) and prefrontal cortex may underlie behavioral impairments in FASD, only one published paper to date has examined the impact of developmental alcohol exposure (AE) on the region responsible for coordinated prefrontal-hippocampal activity: thalamic nucleus reuniens (Re). In the current study, we used a rodent model of human third trimester AE to examine both the acute and lasting impact of a single-day AE on Re. We administered 5.25 g/kg of ethanol to male and female Long Evans rat pups on postnatal day (PD) 7. We used unbiased stereological estimation to evaluate cell death or cell loss at three time points: 12 h after alcohol administration; 4 days after alcohol administration (i.e., PD11); in adulthood (i.e.,PD 72). AE on PD7 increased apoptotic cell death in Re on PD7, and caused short-term cell loss on PD11. This relationship between short-term cell death versus cell number suggests that alcohol-related cell loss is driven by induction of apoptosis. In adulthood, alcohol-exposed animals displayed permanent cell loss (mediating volume loss in the Re), which included a reduction in neuron number (relative to procedural controls). Both procedural controls and alcohol exposed animals displayed a deficit in non-neuronal cell number relative to typically-developing controls, suggesting that Re cell populations may be vulnerable to early life stress as well as AE in an insult- and cell type-dependent manner.
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.