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dc.contributor.advisor Carter, Rosalee C. en
dc.contributor.author Nguyen, Amanda Waber en
dc.date.accessioned 2014-12-05T17:53:09Z en
dc.date.available 2014-12-05T17:53:09Z en
dc.date.issued 2014-12-05 en
dc.date.submitted 2014-12-04 en
dc.identifier.uri http://hdl.handle.net/10211.3/131535 en
dc.description Project (M.S. Biological Sciences (Stem Cell))--California State University, Sacramento, 2014. en
dc.description.abstract Understanding the underlying factors that regulate early neurogenesis is essential to identifying inducers of aberrant neurodevelopment linked to autism and schizophrenia. Determination of these factors will eventually yield possible strategies for treatment and preventive measures to ameliorate negative effects of these inducers. Endogenous regulatory mechanisms ensure proper migration and proliferation of neuronal precursor cells, called neural progenitor cells, in the proliferative zone during embryonic cortical neurogenesis. Although all regulatory factors have yet to be determined, microglia in the developing brain have been shown in previous studies to exhibit regulatory function, engulfing neurons and neural progenitor cells to ensure proper developmental patterning. In response to antigen exposure, the maternal immune response (MIA) increases Interleukin-6 levels through binding of Toll-like Receptor 3 for viral antigens and Toll-like Receptor 4 for bacterial endotoxins. The fetus is then exposed to the resulting increased inflammatory cytokines in the mother, which can pass through the placenta and into the fetus. Increased cytokines correlated with an increased propensity for schizophrenia in human studies, especially in cases with a family history of the disease. These clinical observations are supported by rat and mouse studies that indicate MIA negatively impacts neural proliferation and promotes microglial cell activation, resulting in behavioral deficits in offspring. Our hypothesis is that MIA activates microglia and increases cytokines, altering fetal neuroproliferation and migration patterning. Results from in utero electroporation and intraventricular injection labeled radial glial cells indicated expression of TLR3 and TLR4 in the embryonic rat proliferative zone during neurogenesis. An ELISA method was developed for analysis of IL-6 cytokine levels that indicates an inflammatory response, as is seen in maternal immune activation. This evidence would help clarify the observed differences in susceptibility of autism and schizophrenia in human clinical studies and MIA effects on early neurogenesis. The project was conducted in the Noctor Laboratory, MIND Institute, UC Davis College of Medicine. en
dc.description.sponsorship Biological Sciences (Stem Cell) en
dc.language.iso en_US en
dc.subject Autism en
dc.subject Stem cells en
dc.subject Neurodevelopment en
dc.subject Immunology en
dc.subject Schizophrenia en
dc.title Expression of Toll-like Receptors 3 and 4 (TLR3/4) on neural progenitor cells (radial glial cells): is direct immune activation possible in rat embryonic brain with maternal immune activation? en
dc.type Project en

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