Ntrk2/TrkB differentially modulates fear learning and amygdalar synaptic plasticity through specific phosphorylation sites

Abstract

Event Abstract Back to Event Ntrk2/TrkB differentially modulates fear learning and amygdalar synaptic plasticity through specific phosphorylation sites G. Musumeci1*, C. Sciarretta1, 2, A. Rodriguez-Moreno3, M. Banchaabouchi1, V. Negrete-Diaz3, Marco Costanzi4, V. Berno1, A. V. Egorov5, O. Von-Bohlen-Und-Halbach5, Vincenzo Cestari6, Jose Maria Delgado-Garcia3 and L. Minichiello1, 6 1 Mouse Biology Unit, European Molecular Biology Laboratory, Israel 2 Actelion Pharmaceuticals, Department of in vivo Pharmacology-Neurobiology, Switzerland 3 Universidad Pablo de Olavide, Division de Neurociencias, Spain 4 Istituto di Neuroscienze del CNR, Italy 5 University of Heidelberg, Interdisciplinary Center for Neurosciences (IZN), Department of Neuroanatomy, Germany 6 University of Edinburgh, Universita Lumsa, Facolta di Scienze della Formazione, Rome, Italy and Centre for Neuroregeneraion, United Kingdom Understanding the modulation of the neural circuitry of fear is clearly one of the most important aims in neurobiology because of its manifold implications. It has been proven that LTP in amygdala is necessary for fear conditioning to occur and that TrkB is required for this electrophysiological phenomenon to happen as well. The involved circuitry has its integration point in the amygdala which receives synaptic inputs from different sensory structures. Protein phosphorylation in response to external stimuli is considered a major mechanism underlying dynamic changes in neural circuitry. Ntrk2/TrkB neurotrophin receptor tyrosine kinase potently modulates synaptic plasticity and activates signal transduction pathways mainly through two major phosphorylation sites (Y515/Shc-site; Y816/PLCγ-site). To identify the molecular pathways required for fear learning and amygdalar synaptic plasticity downstream of TrkB we have used highly defined genetic mouse models carrying a point mutation at the above phosphorylation sites (Y515F; Y816F) and examined the physiological relevance of pathways activated through these sites during Pavlovian fear conditioning (FC). Through behavioural, electrophysiological and biochemical analysis, we show that Y816F point mutation impairs acquisition of FC, amygdalar synaptic plasticity and CaMKII signalling at synapses. In contrast, Y515F point mutation affects consolidation but not acquisition of FC to tone and PI3K signalling, suggesting that specific phosphorylation-sites of TrkB differentially modulate amygdalar synaptic plasticity. Conference: 41st European Brain and Behaviour Society Meeting, Rhodes Island, Greece, 13 Sep - 18 Sep, 2009. Presentation Type: Poster Presentation Topic: Poster presentations Citation: Musumeci G, Sciarretta C, Rodriguez-Moreno A, Banchaabouchi M, Negrete-Diaz V, Costanzi M, Berno V, Egorov AV, Von-Bohlen-Und-Halbach O, Cestari V, Delgado-Garcia J and Minichiello L (2009). Ntrk2/TrkB differentially modulates fear learning and amygdalar synaptic plasticity through specific phosphorylation sites. Conference Abstract: 41st European Brain and Behaviour Society Meeting. doi: 10.3389/conf.neuro.10.2009.14.030 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 26 Aug 2009; Published Online: 26 Aug 2009. * Correspondence: G. Musumeci, Mouse Biology Unit, European Molecular Biology Laboratory, Monterotondo, Israel, musumeci@embl.it Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers G. Musumeci C. Sciarretta A. Rodriguez-Moreno M. Banchaabouchi V. Negrete-Diaz Marco Costanzi V. Berno A. V Egorov O. Von-Bohlen-Und-Halbach Vincenzo Cestari Jose Maria Delgado-Garcia L. Minichiello Google G. Musumeci C. Sciarretta A. Rodriguez-Moreno M. Banchaabouchi V. Negrete-Diaz Marco Costanzi V. Berno A. V Egorov O. Von-Bohlen-Und-Halbach Vincenzo Cestari Jose Maria Delgado-Garcia L. Minichiello Google Scholar G. Musumeci C. Sciarretta A. Rodriguez-Moreno M. Banchaabouchi V. Negrete-Diaz Marco Costanzi V. Berno A. V Egorov O. Von-Bohlen-Und-Halbach Vincenzo Cestari Jose Maria Delgado-Garcia L. Minichiello PubMed G. Musumeci C. Sciarretta A. Rodriguez-Moreno M. Banchaabouchi V. Negrete-Diaz Marco Costanzi V. Berno A. V Egorov O. Von-Bohlen-Und-Halbach Vincenzo Cestari Jose Maria Delgado-Garcia L. Minichiello Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. 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