Asad Amanat Ali, UQ : "Developmental vitamin D deficiency rat model of Autism Spectrum Disorder"
Speaker:
Asad Amanat Ali (PhD Exit Seminar)
Queensland Brain Institute, University of Queensland
Title: "Developmental vitamin D deficiency rat model of Autism Spectrum Disorder"
Abstract: Emerging evidence suggests that maternal or developmental vitamin D deficiency (DVD-deficiency) is a risk factor for autism. A well-established association has also been found between gestational infection and increased incidence of autism. Postmortem studies have revealed that brains from autistic children have increased inflammatory cytokines. In addition important developmental neurosteroids have been shown to be significantly increased in the amniotic fluid of children who develop autism. Vitamin D has been shown to both promote anti-inflammatory actions in placenta and regulate expression of several steroidogenic enzymes in vitro. Here we investigate the effects of DVD-deficiency on fetal steroidogenesis and placental immune functions. DVD-deficiency was induced by feeding vitamin D deficient diet to female Sprague-Dawley rats for the period of 6 weeks before mating. Foetuses were collected at gestational day 18 according to their position within the uterus. The expression of steroidogenic enzymes and steroid levels were examined in foetal brain and placenta. Baseline and placental response to the inflammatory agents lipopolysaccharides and polyinosinic-polycytidylic acid (poly I:C) were also examined. A behavioural test battery was conducted to model ASD-like behavioural phenotypes in DVD-deficient animals at different ages to correlate the age of onset of ASD symptoms in humans. DVD-deficiency altered expression of some important steroidogenic enzymes and increased levels of testosterone and corticosterone in foetal brains. In placenta, DVD-deficiency reduced expression of catechol-O-methyltransferase. DVD-deficiency did not affect baseline cytokines in brain or placenta. However when activated with poly I:C, DVD-deficient placentas from male fetuses had higher concentration of IL-6 and 1L-1β then control placentas. The behavioural results of this study reflect some developmental symptoms seen in young children with autism. Using this epidemiologically proven risk factor in an animal model of autism creates the potential to evaluate causative pathways for potential future intervention.
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