Evidence map›Paper›PMID 41207612›Full record

ArticleNeuropharmacology2026

Prenatal alcohol exposure induces circular and linear long non-coding RNAs, and protein-coding genes linked to proinflammatory neuroimmune function, promoting nerve injury-induced allodynia following morphine treatment.

Ariana N Pritha, Andrea A Pasmay, Alissa N Jones, Justin R Carter, Shahani Noor

Abstract read
In one paragraph

Article in Neuropharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Ariana N PrithaDepartment of Neurosciences, University of New Mexico School of Medicine, Albuquerque (city), United States.
Andrea A PasmayDepartment of Neurosciences, University of New Mexico School of Medicine, Albuquerque (city), United States.
Alissa N JonesDepartment of Neurosciences, University of New Mexico School of Medicine, Albuquerque (city), United States.
Justin R CarterDepartment of Neuroscience, University of Arizona, Tucson (city), United States.
Shahani NoorDepartment of Neurosciences, University of New Mexico School of Medicine, Albuquerque (city), United States. Electronic address: snoor@salud.unm.edu.

Funding

Understanding neurophysiological deficits in response inhibition in children with FASDP50AA022534 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Carlos Fernando Valenzuela · 2014 to 2026
$21.5M
Prenatal alcohol exposure generates vulnerability to the proinflammatory effects of morphine and adverse neuroimmune consequencesR01AA029694 · NIAAA · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Shahani Noor · 2022 to 2026
$1.9M
U-Rise at the University of New MexicoT34GM145428 · NIGMS · UNIVERSITY OF NEW MEXICO · PI Cristina D. Takacs-Vesbach · 2022 to 2026
$1.7M
NIAAA NIH HHS P50 AA022534NIAAA NIH HHS R01 AA029694NIGMS NIH HHS T34 GM145428
6 · The paper itself

Abstract

Prenatal alcohol exposure (PAE) exerts lingering effects on neuroimmune function. Based on existing literature on overlapping neuroimmune actions of PAE and opioid pain therapies, here, we examined pain sensitivity (allodynia) in adult male PAE mice following opioid (morphine) treatment. Using a previously characterized model of minor nerve injury, we show that morphine treatment promotes allodynia in PAE mice, not in control mice. This study characterized spinal transcriptomics and explored potential roles of non-coding RNAs (ncRNAs) underlying this paradoxical effect of morphine in PAE mice. Utilizing next-generation bulk RNA sequencing, we generated a comprehensive profile of spinal mRNAs, circular RNAs (circRNAs), and linear long non-coding RNAs (lncRNAs) from morphine-treated allodynic PAE mice. This unbiased approach identified endogenous immune activators (Tcf7l2, Dnaj1, Hmgb1, Hsph1) and the involvement of oxidative stress, hemoglobin genes in PAE mice. Furthermore, a unique spinal circRNA and lncRNA profile, featuring >200 differentially expressed ncRNAs, emerged from morphine-treated PAE mice. Notably, lncRNA and circRNAs with proinflammatory roles, such as circPan3, circRab11, and lncSnhg14, were upregulated, whereas circNr3c2 and circAnkrd12, which are known to exert protective roles against inflammation, were downregulated in PAE mice. Pathways and interaction analysis revealed that these genes are linked to inflammation, cellular stress response, and neuronal-glial interactions that may contribute to pain pathophysiology. Together, these data provide preclinical evidence that PAE and morphine interaction involves spinal proinflammatory activation and are predictive of adverse responses to opioid pain therapy. Dysregulation of ncRNAs may play novel mechanistic roles in neuroimmune dysfunction and allodynic susceptibility under PAE conditions.

Indexed as

HyperalgesiaNeuroinflammatory DiseasesPrenatal Exposure Delayed EffectsAnimalsDown-RegulationEthanolFemaleFetal Alcohol Spectrum DisordersMaleMiceMice, Inbred C57BLMorphinePregnancyRNA, CircularRNA, Long NoncodingSpinal CordEthanolMorphineRNA, CircularRNA, Long NoncodingcircRNAInflammationlncRNAMorphineNeuroimmunePainPrenatal alcohol

Identifiers

PMID41207612
PMCPMC12706847

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.