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Indoor Flame Retardants Disrupt Dendritic Growth In Primary Cortical Cultures By Interfering With Thyroid And Vasopressin Receptor Signaling | 5806
ISSN: 2161-0495

Journal of Clinical Toxicology
Open Access

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Indoor flame retardants disrupt dendritic growth in primary cortical cultures by interfering with thyroid and vasopressin receptor signaling

International Toxicology Summit & Expo

Margarita C. Curras-Collazo, Nichol R., Oh S., Moore T., Murphy T., Lulla A., Ornelas R., Wang A., Calma R, Demissie D., Pontrello C. and Ethell I

ScientificTracks Abstracts: J Clinic Toxicol

DOI: 10.4172/2161-0495.S1.002

Abstract
I ndoor flame retardants such as polybrominated diphenyl ethers (PBDEs) are persistent in the environment, wildlife, and human breast milk and are associated with lower IQ scores and attention deficits in children. In experimental animals PBDEs impair behavior, learning and memory. We examined the effects of the pentaBDE mixture DE-71 (gift of P.R. Kodavanti) and PBDE-99 (gift of L. Dencker) in DIV 5-8 dissociated cortical cultures. In controls main dendrite length increased by 27.2 % at 48h (p<0.001; n=210). Dendrite growth was evident but reduced in sham cultures treated with DMSO (0.03%). Treatment with triiodothyronine (T3; 100 ng/ml) enhanced maturation at 48 and 72h (p<0.05). Main dendrite lengths for T3 at 0h, 24h, and 48h were 89.0+6.9, 108.5+6.9, 144.3+6.9 μm (n=107). Co-treatment with 60 μM DE-71 significantly counteracted the pro-dendritic effects of T3 by 55.0% at 48h (p<0.001, n=88). Similarly, combined treatment with a V1a agonist (10 uM) and DE-71 (60 μM) significantly reduced main dendrite length (at 72h) vs. V1a or DE-71 alone groups. DE-71 alone was pro-dendritic (at 72h) (p<0.001). In contrast, PBDE-99 reduced dendrite growth by 37.3 and 48.0% at 0.03 and 3 μM (p<0.001, n=216). Scholl analysis on neurons transfected with GFP indicated that dendritic branching increased with time and decreased with distance from soma. V1a treatment increased branching while co-treatment with DE-71 produced a sharp decline. These results suggest that PBDEs may interfere with neuronal maturation, in part, by disrupting neurotrophic receptor signaling.
Biography

Margarita C. Curras-Collazo completed her Ph.D in Medical Physiology from The Ohio State University and postdoctoral studies in neuropharmacology at the University of North Carolina, Chapel Hill and at Emory University. She is an Associate Professor of Neuroscience in the Department of Cell Biology & Neuroscience at the University of California, Riverside. Research in the Curras-Collazo lab focuses on transcellular and biochemical mechanisms underlying neurosecretion in the neuroendocrine hypothalamus as well as the neurotoxicological and endocrine disruptive effects of environmental pollutants such as brominated flame retardants. She has published more than 35 papers in reputed journals and has served as an ad hoc reviewer for the National Science Foundation, American Heart Association, and Department of Defense as well as international agencies

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