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[Abstract Title]. - Society for Neuroscience

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immunohistochemisty revealed that the up-regulated expression of NRP-1 and VEGF occurred<br />

in the entorhinally denervated dentate out molecular layer and hippocampal stratum lacunosummolecular<br />

layer, and reactive astrocytes co-expressed both of them. Meanwhile NRP-1 was also<br />

expressed by the neuritis in the denervated area and the granule cells and its processes, which<br />

most likely belong to sprouting axons and/or regrowing dendrites. Double labeling of NRP-1 and<br />

GAP-43 also demonstrated the clustered expression of NRP-1 by regenerated axonal terminals<br />

surrounding the VEGF positive reactive astrocytes. Our data indicates that spatiotemporal shift<br />

of a balance from Sema3A/NRP-1 to VEGF/NRP-1 facilitates the layer-specific neurite<br />

outgrowth and circuits reorganization in the deafferented hippocampus and the crosstalk between<br />

neurons and reactive astrocytes may be involved in the plasticity events of the adult brain after<br />

injury.<br />

Disclosures: W. Wang, None; C. Zhou, None.<br />

Poster<br />

241. Glial Neuronal Interactions<br />

Time: Sunday, November 16, 2008, 1:00 pm - 5:00 pm<br />

Program#/Poster#: 241.23/H5<br />

Topic: B.11.a. Synapses<br />

Support: NSERC<br />

<strong>Title</strong>: Role of astrocyte FMRP on synapse development in Fragile X Syndrome<br />

Authors: *S. STEAD, M. NATHWANI, U. SHETH, L. C. DOERING;<br />

Pathology & Mol. Med., McMaster Univ., Hamilton, ON, Canada<br />

<strong>Abstract</strong>: Fragile X Syndrome (FXS) is the most common cause of inherited mental impairment<br />

that affects approximately 1 in 2000 males and 1 in 4000 females. FXS is caused by a<br />

trinucleotide repeat expansion in the FMR1 gene, resulting in gene silencing and lack of the<br />

protein product termed Fragile X Mental Retardation Protein (FMRP). Abnormal synapse<br />

morphology and function may contribute to the clinical features of FXS.<br />

We recently reported the expression of FMRP in cells of the astrocyte lineage (Pacey and<br />

Doering, 2007). Glial cells are known to play integral roles in the development and maintenance<br />

of synapses in the CNS. We there<strong>for</strong>e examined if neuronal process <strong>for</strong>mation and synapse<br />

development are affected by FMRP in astrocytes. To address this question we utilized a coculture<br />

system of astrocytes and neurons as described by Kaech & Banker (2006), with<br />

modifications. Hippocampal neurons (E16-E17) and cortical astrocytes (P0-P1) were<br />

independently isolated from FMR1 knock out or wild type mice to establish the combinations of

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