Postnatal choline supplementation rescues deficits in synaptic plasticity following prenatal ethanol exposure

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dc.contributor.authorGrafe, Erin L.
dc.contributor.authorWade, Mira M. M.
dc.contributor.authorHodson, Claire E.
dc.contributor.authorThomas, Jennifer D.
dc.contributor.authorChristie, Brian R.
dc.date.accessioned2022-10-28T19:36:42Z
dc.date.available2022-10-28T19:36:42Z
dc.date.copyright2022en_US
dc.date.issued2022
dc.description.abstractPrenatal ethanol exposure (PNEE) is a leading cause of neurodevelopmental impairments, yet treatments for individuals with PNEE are limited. Importantly, postnatal supplementation with the essential nutrient choline can attenuate some adverse effects of PNEE on cognitive development; however, the mechanisms of action for choline supplementation remain unclear. This study used an animal model to determine if choline supplementation could restore hippocampal synaptic plasticity that is normally impaired by prenatal alcohol. Throughout gestation, pregnant Sprague Dawley rats were fed an ethanol liquid diet (35.5% ethanol-derived calories). Offspring were injected with choline chloride (100 mg/kg/day) from postnatal days (PD) 10–30, and then used for in vitro electrophysiology experiments as juveniles (PD 31–35). High-frequency conditioning stimuli were used to induce long-term potentiation (LTP) in the medial perforant path input to the dentate gyrus of the hippocampus. PNEE altered synaptic transmission in female offspring by increasing excitability, an effect that was mitigated with choline supplementation. In contrast, PNEE juvenile males had decreased LTP compared to controls, and this was rescued by choline supplementation. These data demonstrate sex-specific changes in plasticity following PNEE, and provide evidence that cholinerelated improvements in cognitive functioning may be due to its positive impact on hippocampal synaptic physiology.en_US
dc.description.reviewstatusRevieweden_US
dc.description.scholarlevelFacultyen_US
dc.description.sponsorshipThis research is supported by an NIH grant from the National Institute on Alcohol Abuse and Alcoholism AA012446 to JDT and a CIHR award to BRC (FRN 175417). ELG is supported by an NSERC CGS-D.en_US
dc.identifier.citationGrafe, E., Wade, M., Hodson, C., Thomas, J., & Christie, B. (2022). “Postnatal choline supplementation rescues deficits in synaptic plasticity following prenatal ethanol exposure.” Nutrients, 14(10), 2004. https://doi.org/10.3390/nu14102004en_US
dc.identifier.urihttps://doi.org/10.3390/nu14102004
dc.identifier.urihttp://hdl.handle.net/1828/14358
dc.language.isoenen_US
dc.publisherNutrientsen_US
dc.subjectprenatal ethanol exposureen_US
dc.subjectfetal alcoholen_US
dc.subjecthippocampusen_US
dc.subjectsynaptic plasticityen_US
dc.subjectcholine supplementationen_US
dc.subjectdentate gyrusen_US
dc.subjectsex differencesen_US
dc.subjectinterventionen_US
dc.titlePostnatal choline supplementation rescues deficits in synaptic plasticity following prenatal ethanol exposureen_US
dc.typeArticleen_US

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