CELL BIOLOGY OF THE NEURON Polarity ... - Tavernarakis Lab

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Cell Biology of the Neuron: <strong>Polarity</strong>, Plasticity and Regeneration, Crete 2011 NMDA Receptor Regulates Migration of Newly Generated Neurons in the Adult Hippocampus via Disrupted-In-Schizophrenia 1 (DISC1) Takashi Namba 1 , Shigeo Uchino 2 , Kohsaka Shinichi 2 , Kaibuchi Kozo 1 1 Department of Cell Pharmacology, Nagoya University Graduate School of Medicine 2 Department of Neurochemistry, National Institute of Neuroscience In the mammalian brain, new neurons are continuously generated throughout life in the dentate gyrus (DG) of the hippocampus. Previous studies have established that newborn neurons migrate a short distance to be integrated into a pre-existing neuronal circuit in the hippocampus. How the migration of newborn neurons is governed by extracellular signals, however, is not fully understood. Here, we report that N-methyl-D-aspartate receptor (NMDA-R)-mediated signaling is essential for the proper migration and positioning of newborn neurons in the DG. An injection of the NMDA-R antagonists into adult male mice caused the aberrant positioning of newborn neurons, resulting in an overextension of their migration in the DG. Interestingly, we revealed that the administration of NMDA-R antagonists led to a decrease in the expression of Disrupted-In- Schizophrenia 1 (DISC1), a candidate susceptibility gene for major psychiatric disorders such as schizophrenia, which is also known as a critical regulator of neuronal migration in the DG. Furthermore, the overextended migration of newborn neurons induced by the NMDA-R antagonists was significantly rescued by the exogenous expression of DISC1. Collectively, these results suggest that the NMDA-R signaling pathway governs the migration of newborn neurons via the regulation of DISC1 expression in the DG. Presented by: Namba, Takashi Poster No 078 Blue Session 160
Cell Biology of the Neuron: <strong>Polarity</strong>, Plasticity and Regeneration, Crete 2011 Cytoplasmic Linker Proteins Regulate Neuronal Polarization through Microtubule and Growth Cone Dynamics Dorothee Neukirchen, Frank Bradke Max Planck Institute for Neurobiology Axon formation is a hallmark of initial neuronal polarization. This process is thought to be regulated by enhanced microtubule stability in the subsequent axon and changes in actin dynamics in the future axonal growth cone. Here, we show that the microtubule end-binding proteins Cytoplasmic Linker Protein (CLIP) 115 and CLIP 170 were enriched in the axonal growth cone and extended into the actin rich domain of the growth cone. CLIPs were necessary for axon formation and sufficient to induce an axon. The regulation of axonal microtubule stabilization by CLIPs enabled the protrusion of microtubules into the leading edge of the axonal growth cone. Moreover, CLIPs positively regulated growth cone dynamics and restrained actin arc formation, which was necessary for axon growth. In fact, in neurons without CLIP activity, axon formation was restored by actin destabilization or myosin II inhibition. Together, our data suggest that CLIPs enable neuronal polarization by controlling the stabilization of microtubules and growth cone dynamics. Presented by: Neukirchen, Dorothee 161 Poster No 079 Red Session
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The meeting was funded in part by E
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These abstracts should not be cited
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CYFIP1, a Neuronal eIF4E‐BP, Link
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POSTER ABSTRACTS Poster # [‐R(ed)
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030‐B Paracrine Pax6 Activity Reg
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058‐R Dynein Light Chain LC8 is a
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088‐R Spectraplakins ‐ Cytoskel
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121‐R Calmyrin1 Binds to SCG10 Pr
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18.00 ‐ 18.15 Non Hyperpolarizing
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10.00 ‐ 10.30 Neurotrophin Regula
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SESSION 10 SYNAPTOGENESIS Chairpers
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da F. Costa, L. 119 D'Adamo, P. 108
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Lewallen, K. 145 Li, Y.‐H. 201 Li
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Teuling, E. 141 Thiebes, K. 87 Thom
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Cell Biology of the Neuron: Polarit
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Prof. Graeme W. Davis University of
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Prof. Zhigang He Harvard Medical Sc
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Dr. Bernhard Lohkamp Karolinska Ins
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Mr. Abhishek Shrikant Sahasrabudhe
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Dr. Med. Andreas Vlachos Goethe‐U
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