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Maryann Ahenfowah Obiorah
B.S., Montclair State University - 2008
Thesis Advisors: Emanuel DiCicco-Bloom, M.D.
Graduate Program in Neuroscience
CABM - Room 010
Wednesday, July 2, 2014
The developing brain is sensitive to environmental toxicants that can act as teratogens, which are substances that cause malformations during development. One of these is methylmercury (MeHg), to which humans are exposed when consuming contaminated seafood. Prenatal exposure is associated with learning, memory and intelligence deficits in children. These deficits can result from dysfunction in hippocampal neurogenesis – the birth of new neurons.
The period of developmental vulnerability and long-term consequences of low MeHg exposure on future neurogenesis is not clear. We hypothesized that MeHg targets proliferating hippocampal neural precursors in prepubescent (postnatal day 14 – P14) and adolescent (P21) rats. To test our hypothesis, we characterized the effect of MeHg on proliferating neural precursors at different developmental periods and found that MeHg reduces mitotic S-phase cells and Sox2+ neural stem cells at P14, but not at P21. In addition, we determined the effects of a single, early exposure on adolescent neurogenesis by using an age that corresponds to the third trimester of human development (P7). We discovered that early exposure leads to a deficit in proliferating NSCs and newborn neurons at P21. Lastly, we evaluate the molecular mechanism of MeHg-induced deficits by studying the role of microglia-derived reactive oxygen species in MeHg-induced insult. We conclude that MeHg vulnerability is specific to a developmental period that ends at adolescence and that juveniles suffer reduced neurogenesis as a consequence of early exposure, which might contribute to altered hippocampal function.