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Intergenerational Impact of Maternal Traumatic Brain Injury: Distinct Prenatal and Postnatal Contributions and Pharmacological Rescue

Poster Session F - Tuesday, March 10, 2026, 8:00 – 10:00 am PDT, Fairview/Kitsilano Ballroom

Anatoly Martynyuk¹ (), Zeeshan Khan, Ling-Sha Ju, Caleb Charles; ¹University of Florida

Traumatic brain injury (TBI), common among young adults, can cause neurocognitive decline, with emerging epidemiological evidence of psychiatric vulnerabilities in offspring, particularly sons. Mechanisms remain unclear, and no treatments exist. We hypothesized that downregulating stress and inflammatory responses in TBI-affected mothers would mitigate abnormalities in both mothers and offspring, with maternal influence occurring prenatally and via postnatal interaction. Female rats (F0) received moderate TBI via midline fluid percussion injury on day 60 (P60) (F0F_T group). A subset received bumetanide (NKCC1 inhibitor; F0F_TB) before TBI. On P90, they were bred to produce F1 offspring. Half of each litter was reared by biological mothers and half by foster dams, either TBI-affected or unaffected. F0F_T rats showed elevated stress and inflammatory signaling without significant changes in weight, gut microbiome, or behavior. Male offspring of TBI mothers raised by their biological mothers had lower weight at birth and weaning, elevated stress and inflammatory signaling, gut microbiota dysbiosis, and behavioral impairments. Control-born offspring raised by TBI mothers were unaffected. TBI-born offspring raised by control mothers were rescued but still differed from controls in two measures, suggesting that TBI mothers’ postnatal behavior is not abnormal enough to cause deficits in healthy pups, yet not normal enough to rescue TBI pups. Female offspring showed similar trends in weight and anxiety but were otherwise unaffected. Bumetanide prevented both F0 and F1 abnormalities. These findings suggest that maternal TBI influences offspring phenotype primarily through prenatal mechanisms, partially modifiable by postnatal interaction, and that maternal bumetanide mitigates abnormalities across generations.

Topic Area: LONG-TERM MEMORY: Development & aging