ArticleFrontiers in pharmacology2025
The regulation and mechanism of the cAMP-PKA pathway on PTSD-like behaviors exacerbated by alcohol exposure.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed.
- Single prolonged stress in mice: interactions between alcohol drinking, negative affect, and fear learning.Psychopharmacology · 2026Article
- Activation of GLP-1R ameliorates alcohol withdrawal induced anxiety-like behavior by regulating neuronal mitochondrial quality control.Frontiers in pharmacology · 2026Article
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Authors and funding
6 authors.
Funding
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Abstract
Background: Alcohol use disorder (AUD) and post-traumatic stress disorder (PTSD) exhibit a significant degree of comorbidity. Nevertheless, the specific effects and underlying mechanisms by which alcohol, as a risk factor, contributes to the development of PTSD-ike phenotypes remain poorly understood. Both chronic alcohol consumption and exposure to traumatic stress can lead to synaptic damage in the hippocampus, potentially serving as a neurobiological basis for the exacerbation of PTSD induced by alcohol. Methods: In this study, an animal model was established by allowing mice to voluntarily consume alcohol for 2 weeks, followed by exposure to a single prolonged stress combined with foot shock (SPS&FS). Subsequently, the mice received an intraperitoneal injection of rolipram (1 mg/kg), and behavioral, biochemical, and morphological analyses were performed. Results: The findings revealed that individuals with early alcohol exposure exhibited more pronounced deficits in fear extinction during the fear extinction task (FET) and displayed higher levels of anxiety-like behavior in both the open field test (OFT) and the elevated plus maze test (EPM). Activation of cAMP-PKA signaling enhanced the downregulation of brain-derived neurotrophic factor (BDNF) and tyrosine kinase receptor B (TrkB), upregulated the expression of PSD95, synaptophysin, AMPA, and NMDA receptor subtypes, and reversed the impairment of CA1 synaptic function and dendritic structure in the hippocampus. Conclusion: Activation of the cAMP-PKA pathway facilitated fear extinction in PTSD mice with early alcohol exposure, alleviated anxiety-like behavior, attenuated symptoms of AUD following ethanol relapses. These findings suggest that modulating hippocampal synaptic plasticity by activating the cAMP-PKA pathway may represent a promising therapeutic approach for attenuating alcohol-exacerbated PTSD-like behaviors.
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