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P2.85: Morphometry and connectivity of corpus callosum in Williams syndrome: Indexes of neural development
Author(s) -
Sampaio A.,
Bouix S.,
Sousa N.,
Prieto M.,
Vasconcelos C.,
Shenton M.
Publication year - 2010
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2010.07.215
Subject(s) - splenium , corpus callosum , rostrum , fractional anisotropy , diffusion mri , anatomy , white matter , neuroscience , brain size , psychology , biology , magnetic resonance imaging , medicine , zoology , radiology , genus
neuronal cytoskeleton. Here, we aim to investigate the molecular mechanisms involved in UCB-induced changes on neuronal cytoskeletal dynamics. Primary cultures of mouse hippocampal neurons were incubated at 1 day-in-vitro (DIV) with 50 M purified UCB plus 100 M human serum albumin for 24 h at 37 ◦C and further cultured until 3 DIV. Axonal elongation was determined by Tau1 immunostaining. Microtubule (MT) dynamics was assessed in neurons expressing pCAG-EB3-EGFP to identify the MT plus end-binding protein 3 (EB3). MAP2, Tau1, kinesin and dynein expression and location along the axon were determined by immunostaining with specific antibodies. In addition, MAP2 and Tau1 binding to MT was assessed after saponin extraction. Mitochondria arrangement along the axon was determined using MitoTracker®. UCB-treated neurons showed a reduced axonal outgrowth (>10%, p < 0.05) and MT polymerization rate (∼30%, p < 0.05). In addition, UCB increased MAP2 axonal entry (∼15% p < 0.01) as well as MAP2 binding to MT (>25%, p < 0.01). Tau1 expression was significantly increased by UCB exposure (>60%, p < 0.01), as well as its binding to MT along the axonal length (>20%, p < 0.01). Interestingly, UCB increased mitochondria aggregation at the distal portion of the axon (>60%, p < 0.05) suggesting a deficient axonal transport. In accordance, preliminary results suggested that UCB reduces both kinesin (∼5%) and dynein (∼15%) motor protein expression along the axon. These findings demonstrated that an exposure of developing neurons to UCB promotes cytoskeleton alterations justifying moderate to severe neurological damage in neonatal jaundiced, which is known to be especially injurious in preterm infants as compared to term newborns. Funded by FCT-PTDC/SAU-NEU/64385/2006 to D.B.