Abstract: | Med-Hank’s balanced salt solution (HBSS) or LPS at E10.5 and collected ical Research Fund.the maternal serum (MS), amniotic fluid (AF), and whole brains fromembryos. The results indicate that IL-6 was elevated within MS [F(3,Central Nervous System Biodistribution of AAV5-GFP Following11) = 870.27, p < 0.001] and amniotic fluid [F(3, 11) = 9.32, p <Intraventricular Administration in Neonatal and Adult Mice0.05], whereas IL-1β, on the other hand, was elevated in the MS [F(3,11) = 8.18, p < 0.001], AF [F(3, 11) = 39.07, p < 0.001], and brain tis-Z. Nan, L. Belur, D. Wolf, R. Gunther, C. Whitley, R. S. McIvor, sue [F(3, 11) = 3.7, p < 0.001]. TNF-α, however, was only found to beand W. C. Low elevated in MS [F(3, 11) = 47.41, p < 0.001]. In addition, nigrostratialcocultures were established from tissue harvested at E14.5 and 72 hlater were exposed to various doses of IL-6, IL-1β, and TNF-α to University of Minnesota, Minneapolis, MN, USAassess the effects of proinflammatory cytokines on expression of neu-rotrophic factors, glial-derived neurotrophic factor (GDNF), and brain- Current treatments for lysosomal storage disorders involve enzymereplacement therapy (ERT) such as iduronidase (IDUA) for treating derived neurotrophic factor (BDNF). The results indicate that after 24 h of treatment, IL-1β produced a statistically significant dose-depen-dent increase in GDNF protein [F(5, 23) = 7.33, p < 0.001, using Tu- fixed, and cut into coronal sections. Immunohistochemical staining oframified microglia was performed using antibody IBA1 and staining key’s post hoc] while TNF-α produced a dose-dependent decrease(p < 0.05) in GDNF. There were no observed dose-dependent changes of activated microglia was performed using MHC class II antibodyOX6. Microglia density (MD) was measured in the gray matter of the in expression of BDNF. In conclusion, these results suggest that expo-sure to prenatal LPS results in increases in proinflammatory cytokines ventral horn region of spinal cord for both cell types. The spinal cordMD was compared between cell-treated, nontreated (media injected), within MS, AF, and brain that can impact the expression of GDNF.Alteration of neurotrophic factors, such as GDNF, during this critical nontreated [cyclosporine (CsA) injected], and C57BL/6J control mice.Consistently reduced ramified microglia density was noted in mice period of nigrostriatal pathway development could result in altered DAcell development, leading to permanent cell loss. Future studies will receiving 25 × 10 6 cells in both the cervical (p < 0.01) and lumbar(p < 0.05) spinal cord. ALS mice injected with the 10 × 10 6 or 50 × further explore the mechanism whereby proinflammatory cytokines al-ters neurotrophic factor expression in the developing nigrostriatal 10 6 cell dose showed no significant differences from nontreated G93Acontrol mice. Surprisingly, exceptionally higher microglia densities pathway. |