Maternal selenium dietary supplementation alters sociability and reinforcement learning deficits induced by in utero exposure to maternal immune activation in mice

Dec 24, 2023Brain, behavior, and immunity

Selenium supplements during pregnancy may reduce social and learning problems caused by prenatal immune activation in mice

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Abstract

Selenium supplementation during pregnancy prevented the elevation of placental IL-1β and IL-17 caused by maternal immune activation.

Maternal immune activation (MIA) is linked to increased levels of inflammatory cytokines in the placenta, which are associated with neurodevelopmental risks in offspring.
Selenium supplementation during pregnancy successfully prevented the increase in placental cytokines induced by MIA.
MIA resulted in elevated calcium levels in the foetal brain, which were mitigated by selenium supplementation.
Selenium supplementation improved sociability in female offspring affected by MIA, but did not restore social memory in male offspring.
Exposure to either poly-I:C or selenium negatively impacted performance in a reinforcement learning task, primarily due to increased exploratory behavior.

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Maternal immune activation (MIA) during pregnancy increases the risk for the unborn foetus to develop neurodevelopmental conditions such as autism spectrum disorder and schizophrenia later in life. MIA mouse models recapitulate behavioural and biological phenotypes relevant to both conditions, and are valuable models to test novel treatment approaches. Selenium (Se) has potent anti-inflammatory properties suggesting it may be an effective prophylactic treatment against MIA. The aim of this study was to determine if Se supplementation during pregnancy can prevent adverse effects of MIA on offspring brain and behaviour in a mouse model. Selenium was administered via drinking water (1.5 ppm) to pregnant dams from gestational day (GD) 9 to birth, and MIA was induced at GD17 using polyinosinic:polycytidylic acid (poly-I:C, 20 mg/kg via intraperitoneal injection). Foetal placenta and brain cytokine levels were assessed using a Luminex assay and brain elemental nutrients assessed using inductively coupled plasma- mass spectrometry. Adult offspring were behaviourally assessed using a reinforcement learning paradigm, the three-chamber sociability test and the open field test. MIA elevated placental IL-1β and IL-17, and Se supplementation successfully prevented this elevation. MIA caused an increase in foetal brain calcium, which was prevented by Se supplement. MIA caused in offspring a female-specific reduction in sociability, which was recovered by Se, and a male-specific reduction in social memory, which was not recovered by Se. Exposure to poly-I:C or selenium, but not both, reduced performance in the reinforcement learning task. Computational modelling indicated that this was predominantly due to increased exploratory behaviour, rather than reduced rate of learning the location of the food reward. This study demonstrates that while Se may be beneficial in ameliorating sociability deficits caused by MIA, it may have negative effects in other behavioural domains. Caution in the use of Se supplementation during pregnancy is therefore warranted.

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Maternal selenium dietary supplementation alters sociability and reinforcement learning deficits induced by in utero exposure to maternal immune activation in mice

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