Evidence map›Paper›PMID 42595055›Full record

ArticleNeurotoxicology2026

Firemaster 550 differentially alters gene expression underlying synaptic function in amygdala of prairie voles after gestational or lactational exposure.

Andrew J Newell, Abdull J Massri, Sagi E Gillera, Jenna M Berger, Vijayalakshmi Panduri, Liwen Liu, Kevin Gerrish, Heather B Patisaul

Abstract read
In one paragraph

Article in Neurotoxicology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Andrew J NewellMechanistic Toxicology Branch, Division of Translation Toxicology, National Institute of Environmental Health Sciences, USA. Electronic address: andrew.newell@nih.gov.
Abdull J MassriNIEHS Integrative Bioinformatics Support Group, Division of Intramural Research, USA.
Sagi E GilleraMechanistic Toxicology Branch, Division of Translation Toxicology, National Institute of Environmental Health Sciences, USA.
Jenna M BergerMechanistic Toxicology Branch, Division of Translation Toxicology, National Institute of Environmental Health Sciences, USA.
Vijayalakshmi PanduriNIEHS Genomics Core, Division of Intramural Research, Epigenetics and RNA Biology Laboratory, USA.
Liwen LiuNIEHS Genomics Core, Division of Intramural Research, Epigenetics and RNA Biology Laboratory, USA.
Kevin GerrishNIEHS Genomics Core, Division of Intramural Research, Epigenetics and RNA Biology Laboratory, USA.
Heather B PatisaulMechanistic Toxicology Branch, Division of Translation Toxicology, National Institute of Environmental Health Sciences, USA.

Funding

Neurodevelopmental effects of flame retardant exposureU01ES035843 · NIEHS · NORTH CAROLINA STATE UNIVERSITY RALEIGH · PI John Meitzen · 2024 to 2026
$1.2M
Endocrine Disruption of the Social BrainZIAES103404 · NIEHS · NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES · PI PATISAUL, HEATHER · 2025 to 2025
$1.1M
Intramural NIH HHS ZIA ES103404NIEHS NIH HHS U01 ES035843
6 · The paper itself

Abstract

Neurodevelopmental disorders often share similar behavioral diagnostic criteria including socioemotional and cognitive deficits. The prairie vole is a uniquely suitable model to study these deficits because they demonstrate strong social affiliation, bi-parental care, and partner attachment. Previously, we have shown that developmental exposure to the flame-retardant mixture Firemaster 550 (FM 550) impairs socioemotional behavior in the prairie vole and alters underlying neuroanatomy and function. However, the mechanisms for impaired pair bonding in males and increased anxiety in females remain unknown, along with the specific critical window(s) of vulnerability. Herein, we exposed prairie vole dams to FM 550 during gestation or lactation, and performed bulk RNA-seq on the amygdala, a hub of socioemotional processing, in their adult offspring. Two mathematically orthogonal methods were utilized for analysis, a linear statistical method and an ensemble machine learning method, incorporating sex as a biological variable. Gene ontology (GO) pathway analysis was performed following both and results compared to identify potential mechanisms of toxicity. GO results indicated consistent expression changes in the Synapse cellular component in all conditions, and implicated glutamatergic signaling specifically. Additionally, gestational exposure (GE) altered genes underlying modulation of synaptic transmission and neural development, while lactational exposure (LE) impacted genes underlying synaptic plasticity, axon guidance, and mitophagy. Machine learning identified disruption of endocrine system development, regulation of biosynthetic processes in GE animals, and suppression of various neuroinflammatory genes across multiple groups. Finally, we performed RNA expression analysis using Nanostring and demonstrated stronger correlation with the differentially expressed genes (DEG) of interest in females than males. Overall, this study demonstrates both the intersecting and distinct impacts of FM 550 exposure on amygdalar gene expression depending on sex and timing of exposure.

Indexed as

AmygdalaGene ExpressionLactationPrenatal Exposure Delayed EffectsSynapsesAnimalsArvicolinaeFemaleMalePregnancyAmygdalaCritical PeriodDevelopmental NeurotoxicologySocial Brain NetworkTranscriptomics

Identifiers

PMID42595055
PMCPMC13528592

What OpenQuestion holds

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Registered trials

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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.