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 Diffusion/Trapping of AMPA Receptors at Neurexin- Neuroligin Adhesions through PSD-95 Magali Mondin 1 , Eric Hosy 1 , Martin Heine 2 , Daniel Choquet 1 , Olivier Thoumine 1 1 IINS CNRS UMR 5297 2 Leibniz institute for neurobiology Neurexin/neuroligin adhesion plays a central role in synapse formation, but the mechanisms linking initial contact to the assembly of functional pre- and postsynaptic macromolecular complexes remain unclear. Here we investigated whether the recruitment of AMPA receptors at early neurexin/neuroligin contacts could occur through a diffusion/trap mechanism. We show by single nanoparticle tracking, that surface-diffusing AMPA receptors in primary hippocampal neurons stop reversibly at PSD-95 clusters triggered by neurexin/neuroligin adhesion. In addition, the accumulation of functional AMPA receptors at new neurexin/neuroligin contacts is prevented upon blocking AMPA receptor surface diffusion by antibody cross-link. Using neuroligin-1 mutants and inhibitory RNAs, we further show that the membrane mobility of AMPA receptors inversely correlates with neuroligin-1 level, and that this effect requires the interaction between neuroligin-1 and PSD-95. The triggering of new neurexin/neuroligin adhesions causes a depletion of PSD-95 from pre-existing synapses, accompanied by a drop in AMPA miniature EPSCs, suggesting a competitive mechanism. Finally, AMPA synaptic transmission is significantly reduced in CA1 hippocampal cells of slices from neuroligin-1 knock-out mice at early developmental stage. Overall, we propose that a pool of membrane-diffusing PSD-95 and AMPA receptors can be rapidly trapped at newly forming neurexin/neuroligin adhesions during post-synapse formation. Presented by: Mondin, Magali Poster No 076 Red Session 158
Cell Biology of the Neuron: <strong>Polarity</strong>, Plasticity and Regeneration, Crete 2011 The End of 35-year Quest has Come by FRET Imaging - the Molecular Mechanism of dbcAMP-Induced Neurite Outgrowth Takeshi Nakamura 1 , Akihiro Goto 2 , Mikio Hoshino 3 , Michiyuki Matsuda 2 1 Research Institute for Biological Sciences, Tokyo University of Science, 2 Graduate School of Biostudies, Kyoto University 3 National Institute of Neuroscience, NCNP The second messenger cAMP plays a pivotal role in neurite/axon growth and guidance, but its downstream pathways leading to the regulation of Rho GTPases, centrally implicated in neuronal morphogenesis, remain elusive. We examined spatiotemporal changes in Rac1 and Cdc42 activity and phosphatidylinositol 3,4,5-triphosphate (PIP3) concentration in dibutyryl cAMP (dbcAMP)-treated PC12D cells using Förster resonance energy transfer-based biosensors. During a 30-min incubation with dbcAMP, Rac1 activity gradually increased throughout the cells and remained at its maximal level. There was no change in PIP3 concentration. After a 5-h incubation with dbcAMP, Rac1 and Cdc42 were activated at the protruding tips of neurites without PIP3 accumulation. dbcAMPinduced Rac1 activation was principally mediated by protein kinase A (PKA) and STEF/Tiam2. STEF depletion drastically reduced dbcAMP-induced neurite outgrowth. PKA phosphorylates STEF at three residues (Thr749, Ser782, Ser1562); T749 phosphorylation was critical for dbcAMP-induced Rac1 activation and neurite extension. During dbcAMP-induced neurite outgrowth, PKA activation at the plasma membrane became localized to neurite tips; this may contribute to local Rac1 activation at the same neurite tips. Considering the critical role of Rac1 in neuronal morphogenesis, the PKA-STEF-Rac1 pathway may play a crucial role in cytoskeletal regulation during neurite/axon outgrowth and guidance which depend on cAMP signals. This work could provide a clue to how to regenerate injured axons. It is because the specific reinforcement at the appropriate point in signaling pathways in addition to cAMP administration is expected to synergistically promote regeneration. Presented by: Nakamura, Takeshi 159 Poster No 077 Green 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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Dr. Christian Alfano INSERM U636, N
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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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