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Introduction: Healthy pregnancy is associated with re-organization of maternal cognitive function that persists through the early postpartum period. In addition, pregnancy is a state of physiological inflammation and oxidative stress that results from complex physiological adaptations such as placentation and vascular remodeling. The objectives of this study were to determine a) the short-term and long-term impact of pregnancy on maternal memory function and neurobiology and b) the relationship between physiological inflammation and oxidative stress with maternal memory function. We hypothesized that pregnant rats have reduced recollective memory and this deficit is associated with pregnancy-induced systemic inflammation and oxidative stress. Methods: Recollective memory was tested using the novel object recognition test in young adult female Sprague Dawley rats of varying reproductive states [non-pregnant (NP), late gestation (PREG, gestational day 20, term = 22-23 days), and two months postpartum (PP); n = 7-8/group]. We measured molecular markers of neuronal activation (early growth response-1, EGR-1), astroglial injury (Glial fibrillary acidic protein, GFAP), and activation of apoptosis-mediated cell death (Caspase-3 activity) in the dorsal CA1 region of the hippocampus via western blotting. Plasma proinflammatory cytokines were measured using a MILLIPLEX® magnetic bead assay, and plasma oxidative stress was measured using the advanced oxidative protein products (AOPP) assay. Results: During late gestation, spatial memory was impacted, as evidenced by decreased recollective memory in the novel object recognition test (latency to initial contact of the novel object, p = 0.018 vs. NP rats). This effect was transient, as no effects on recollective memory was observed two months postpartum (p > 0.05 vs. NP rats). In contrast, pregnancy-associated systemic inflammation (IL-17A: NP = 16.78 ± 3.50 vs PREG = 65.18 ± 17.50 pg/ml, p = 0.013) and oxidative stress (AOPP: NP = 191.9 ± 10.90 μM vs PREG = 278.2 ± 23.30 μM, p = 0.006) were maintained two months postpartum (IL-17A: NP = 20.38 ± 3.65 vs PP = 37.31 ± 7.43 pg/ml, p = 0.047; AOPP: NP = 162.0 ± 24.61 μM vs PP: 285.60 ± 49.19 μM, p = 0.034). This elevated inflammation and oxidative stress did not impact hippocampal neuronal activity (EGR-1, p = 0.650), astrocyte injury (GFAP, p = 0.889), or caspase-3-mediated cell death (p = 0.358). Conclusions: Pregnancy reduces maternal short-term recollective memory function and induces systemic proinflammatory responses and oxidative stress. Transient cognitive deficits during the perinatal period were not associated with impaired hippocampal neuronal activity, suggesting functional impairments in other brain regions associated with memory function, such as the entorhinal cortex. While maternal memory deficits are transient and limited to the perinatal period, markers of maternal systemic inflammation and oxidativ NIH R01HL146562-04S1, AHA 22POST-903250 This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.