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  • Information from Lay-Language Summaries is Embargoed Until the Conclusion of the Scientific Presentation

    244—Developmental Disorders Associated with Prenatal Events

    Sunday, November 10, 2013, 1:00 pm - 5:00 pm

    244.11: Effects of a prenatal vitamin d deficiency on offspring behavior in mice

    Location: Halls B-H

    ">*A. M. BELENCHIA1, K. L. JONES2, M. WILL1, D. Q. BEVERSDORF1, V. VIEIRA-POTTER1, Z. FETTER1, C. A. PETERSON1;
    1Univ. of Missouri, Columbia, MO; 2Univ. of California-Davis, Davis, CA

    Abstract Body: Vitamin D deficiency/insufficiency, defined as inadequate circulating concentrations of 25-hydroxyvitamn D (25OHD), has been estimated to affect up to 75% of pregnant women in some developed nations. Multiple studies have established an associative link between low maternal 25OHD concentrations and a variety of mental health conditions, including autism spectrum disorders (ASD). The current study aimed to examine the effects of prenatal vitamin D deficiency on offspring behaviors. Female C57BL/6J mice were assigned to either a vitamin D deficient diet or a control diet two weeks prior to mating and maintained on this diet throughout pregnancy until postnatal day 7, at which point both dietary groups were switched to the control diet. We subsequently recorded the ultrasonic vocalizations of the offspring on postnatal day 8 as a measure of social communication. Beginning on postnatal day 60, the adult offspring were tested for levels of social interaction using the Crawley 3-chamber social approach task. Anxiety was tested using the elevated-plus maze, and general activity levels were assessed using the open field.

    Lay Language Summary: Our research indicates that vitamin D deficiency during pregnancy does not lead to autistic-like behaviors in offspring. Additionally, while it remains possible that a vitamin D deficient prenatal environment has long-lasting effects in the inflammatory status of offspring, these effects seem to be modest.
    Autism spectrum disorders are a set of neurodevelopmental disorders that are classified by loss of abilities in social interactions, social communication, and the presence of repetitive and restricted interests and behaviors. While the exact cause of autism remains to be determined, it seems a combination of genetic and environmental influences contribute to the development of the disorder. Recently, researchers have hypothesized that a deficiency in vitamin D during pregnancy is associated with a higher risk of developing autism. As no other investigators have determined the effect of prenatal vitamin D status on behaviors related to autism, we aimed to investigate this relationship in a rodent model. Our results suggest that there is no association between prenatal vitamin D deficiency and autism. Additionally, we did not observe the chronic immune irregularities that are often associated with autism.
    To test whether prenatal vitamin D status had any effect on autistic-like behaviors in offspring, we exposed mothers to either a diet deficient in vitamin D or a control diet, which had adequate levels of vitamin D. Mothers were randomly assigned to one of the two diets prior to conception and remained on the diet throughout gestation. After they were weaned from their mothers’ milk, all offspring were placed on the diet containing sufficient vitamin D, effectively limiting the dietary intervention to the prenatal period. To test social communication, vocalizations of young offspring were recorded during social isolation. Then, to test social interactions, adult offspring were tested for time spent with a “stranger” mouse and with an unfamiliar object. Adult offspring were then tested for anxious-like behavior and general activity levels using tasks known as the Elevated-Plus Maze and the Open Field. We found no significant differences across offspring, regardless of prenatal vitamin D status or sex. Further, as immune dysregulation is seen in some individuals with autism, we measured the blood of adult offspring to determine if prenatal vitamin D status had long lasting effects on general inflammation. Out of the eight immune markers measured, only two showed a significant effect of prenatal vitamin D status, with those born to vitamin D deficient mothers having elevated levels of two pro-inflammatory markers.
    These results suggest that despite emerging theories, it does not appear that prenatal vitamin D deficiency leads to the development of autism-like behaviors in offspring. However, it is important to note that prenatal vitamin D deficiency may lead to abnormalities in behaviors not tested in the current study. Further research is needed to determine whether prenatal vitamin D deficiency leads to other cognitive and behavioral deficits in offspring, as well as the mechanisms by which these effects are exerted.

    Information from Lay-Language Summaries is Embargoed Until the Conclusion of the Scientific Presentation

    244—Developmental Disorders Associated with Prenatal Events

    Sunday, November 10, 2013, 1:00 pm - 5:00 pm

    244.11: Effects of a prenatal vitamin d deficiency on offspring behavior in mice

    Location: Halls B-H

    ">*A. M. BELENCHIA1, K. L. JONES2, M. WILL1, D. Q. BEVERSDORF1, V. VIEIRA-POTTER1, Z. FETTER1, C. A. PETERSON1;
    1Univ. of Missouri, Columbia, MO; 2Univ. of California-Davis, Davis, CA

    Abstract Body: Vitamin D deficiency/insufficiency, defined as inadequate circulating concentrations of 25-hydroxyvitamn D (25OHD), has been estimated to affect up to 75% of pregnant women in some developed nations. Multiple studies have established an associative link between low maternal 25OHD concentrations and a variety of mental health conditions, including autism spectrum disorders (ASD). The current study aimed to examine the effects of prenatal vitamin D deficiency on offspring behaviors. Female C57BL/6J mice were assigned to either a vitamin D deficient diet or a control diet two weeks prior to mating and maintained on this diet throughout pregnancy until postnatal day 7, at which point both dietary groups were switched to the control diet. We subsequently recorded the ultrasonic vocalizations of the offspring on postnatal day 8 as a measure of social communication. Beginning on postnatal day 60, the adult offspring were tested for levels of social interaction using the Crawley 3-chamber social approach task. Anxiety was tested using the elevated-plus maze, and general activity levels were assessed using the open field.

    Lay Language Summary: Our research indicates that vitamin D deficiency during pregnancy does not lead to autistic-like behaviors in offspring. Additionally, while it remains possible that a vitamin D deficient prenatal environment has long-lasting effects in the inflammatory status of offspring, these effects seem to be modest.
    Autism spectrum disorders are a set of neurodevelopmental disorders that are classified by loss of abilities in social interactions, social communication, and the presence of repetitive and restricted interests and behaviors. While the exact cause of autism remains to be determined, it seems a combination of genetic and environmental influences contribute to the development of the disorder. Recently, researchers have hypothesized that a deficiency in vitamin D during pregnancy is associated with a higher risk of developing autism. As no other investigators have determined the effect of prenatal vitamin D status on behaviors related to autism, we aimed to investigate this relationship in a rodent model. Our results suggest that there is no association between prenatal vitamin D deficiency and autism. Additionally, we did not observe the chronic immune irregularities that are often associated with autism.
    To test whether prenatal vitamin D status had any effect on autistic-like behaviors in offspring, we exposed mothers to either a diet deficient in vitamin D or a control diet, which had adequate levels of vitamin D. Mothers were randomly assigned to one of the two diets prior to conception and remained on the diet throughout gestation. After they were weaned from their mothers’ milk, all offspring were placed on the diet containing sufficient vitamin D, effectively limiting the dietary intervention to the prenatal period. To test social communication, vocalizations of young offspring were recorded during social isolation. Then, to test social interactions, adult offspring were tested for time spent with a “stranger” mouse and with an unfamiliar object. Adult offspring were then tested for anxious-like behavior and general activity levels using tasks known as the Elevated-Plus Maze and the Open Field. We found no significant differences across offspring, regardless of prenatal vitamin D status or sex. Further, as immune dysregulation is seen in some individuals with autism, we measured the blood of adult offspring to determine if prenatal vitamin D status had long lasting effects on general inflammation. Out of the eight immune markers measured, only two showed a significant effect of prenatal vitamin D status, with those born to vitamin D deficient mothers having elevated levels of two pro-inflammatory markers.
    These results suggest that despite emerging theories, it does not appear that prenatal vitamin D deficiency leads to the development of autism-like behaviors in offspring. However, it is important to note that prenatal vitamin D deficiency may lead to abnormalities in behaviors not tested in the current study. Further research is needed to determine whether prenatal vitamin D deficiency leads to other cognitive and behavioral deficits in offspring, as well as the mechanisms by which these effects are exerted.