ArticleScientific reports2026
Acute pretrauma ethanol exacerbates PTSD-like phenotype in rats and is reversed by early intranasal ketamine.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alcohol consumption before trauma is a prevalent but understudied risk factor for posttraumatic stress disorder (PTSD). This study investigated whether acute ethanol exposure prior to trauma modulates PTSD-like symptom development in rats, identified hippocampal mechanisms involved, and tested an early post-trauma intervention. Adult male Sprague-Dawley rats received ethanol (1.6 g/kg, 40% v/v, intraperitoneal) or saline 4 h or 30 min before predator scent stress (PSS) or sham-PSS exposure. Seven days post-exposure, anxiety-like behavior (elevated plus-maze), acoustic startle response, and cue-induced freezing were assessed using validated cut-off behavioral criteria to classify PTSD-like phenotypes. Hippocampal CA1 dendritic morphology was examined in relation to behavioral outcomes. In parallel cohorts, immunofluorescence quantified hippocampal hyperpolarization-activated cyclic nucleotide-gated channel 1 (HCN1), neuropeptide Y (NPY), NPY-Y1 receptor (NPY-Y1-R), and brain-derived neurotrophic factor (BDNF) 1 h post-PSS. A separate ethanol-pretreated group received subanesthetic intranasal ketamine (0.6 mg/kg) via amylolipid nanovesicles (ketamine-ALN) 1 h after PSS. Rats administered ethanol 4 h-but not 30 min-before PSS showed a higher prevalence of PTSD-like phenotypes at 7 days and significantly greater CA1 dendritic retraction. Combined ethanol and PSS exposure was associated with reduced BDNF and NPY levels, increased HCN1, and loss of NPY-Y1-R immunoreactivity, consistent with a hypoexcitable, plasticity-resistant state in the hippocampus. Rats that received early post-PSS ketamine-ALN showed lower cue-induced freezing, a more resilient behavioral profile, and less dendritic atrophy than unloaded-ALN-treated rats. Pre-trauma timed ethanol exposure was associated with a hippocampal "double-hit" involving HCN1 and NPY-Y1-R circuits, together with greater PTSD-like vulnerability. A single early post-trauma intranasal subanesthetic dose of ketamine was associated with a lower prevalence of PTSD-like phenotype, suggesting a promising preventive strategy for alcohol-exposed trauma survivors.
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.