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CORTICO-ACCUMBAL TRANSCRIPTOMIC ALTERATIONS FOLLOWING FETAL GROWTH RESTRICTION UNDERLIE SEX-SPECIFIC ATTENTION-DEFICIT/HYPERACTIVITY DISORDER (ADHD)-LIKE BEHAVIORS
Patricia Migueland 15 co-authors
Douglas Research Centre
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS07-10AM-498
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Date TBA
Board: PS07-10AM-498
Event Information
Poster Board
PS07-10AM-498
Poster
View posterAbstract
Fetal growth restriction (FR) is associated with increased risk for attention-deficit/hyperactivity disorder (ADHD), a neurodevelopmental condition with higher prevalence in males, yet the molecular basis of this sex-specific vulnerability remains unclear. We examined the impact of FR on ADHD-like behaviors in adulthood and the associated transcriptomic alterations within the medial prefrontal cortex (mPFC) and nucleus accumbens (NAcc), regions involved in executive function and locomotion/motivation. Sprague Dawley dams were assigned to control or food restriction (FR) groups on gestational day 10. Adult offspring were assessed using the open field (OF) and attentional set-shifting task (ASST; n=10–12/group), and another cohort was used for bulk RNA-sequencing (n=9–10/group/sex/region). FR males, but not females, exhibited hyperactivity in the OF, reflected by increased mobility. In contrast, FR females showed initial rule discrimination impairments in the ASST, with no deficits in strategy shifting. Transcriptomic analyses revealed marked sex- and region-specific effects of FR. In the mPFC, FR induced 355 differentially expressed genes (DEGs) in females and 309 in males, with minimal overlap. In the NAcc, 300 DEGs were identified in females and 417 in males (24 overlapping). Pathway analyses identified WNT/β-catenin signaling as a common FR-affected pathway across sexes and regions. In contrast, lipid metabolism pathways were uniquely altered in the female mPFC, while male-specific NAcc changes were enriched for neurophysiological processes, including opioid receptor signaling and intrinsic membrane excitability. Together, these findings show that FR induces sex-specific ADHD-like phenotypes linked to distinct cortico-accumbal transcriptomic signatures.
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