Abstract
Event Abstract Back to Event Role of TRPC1 ion channel in hippocampal neurons Sophie Lepannetier1*, Olivier Schakman1, Francois Seghers1 and Philippe Gailly1 1 Université catholique de Louvain, Institute of Neuroscience, Belgium Transient receptor potential canonical 1 (TRPC1) is a non selective cation channel. It is involved in stored-operated Ca2+ entry in cooperation with Orai channel and activated by STIM1, a sensor of Ca2+ contents in the endoplamic reticulum. However, several pieces of evidence suggest that TRPC1 can be activated independently of store depletion in response to agonists. Using LacZ reporter mouse, we found that TRPC1 is abundantly expressed in neurons from CA1-CA3 regions and to a lesser extent from the dentate gyrus region of the hippocampus. We compared cellular culture of hippocampal neurons from Trpc1-/- mice to wild type mice. Interestingly, stimulation with dihydroxyphenylglycine (DHPG), an agonist of group I metabotropic glutamate receptors (consisting of mGluR1 and mGluR5) induced a store-independent entry of Ca2+ that was very much reduced in hippocampal neurons from Trpc1-/- mice. Studying brains slices, we observed that LTP in Schaffer collaterals-CA1 synpases was diminished in Trpc1-/- mice when induced with a mild stimulus (theta burst consisting of 4 stimuli at 100Hz repeated at 5 Hz during 1s). Cognition tests such as Modified Y maze and contextual fear conditioning, realized on 4-8 months old mice revealed a deficit memory. Moreover, we noted that the specific hippocampal overexpression of the immediate early gene zif268 related to new environment learning was blunted in Trpc1-/- mice. We conclude that TRPC1 channels are activated by mGluR5 stimulation and play a role in neuronal plasticity. Keywords: TRPC1, mGluR, Hippocampus, Neuronal Plasticity, Memory Conference: 12th National Congress of the Belgian Society for Neuroscience, Gent, Belgium, 22 May - 22 May, 2017. Presentation Type: Poster Presentation Topic: Neural Excitability, Synapses, and Glia: Cellular Mechanisms Citation: Lepannetier S, Schakman O, Seghers F and Gailly P (2019). Role of TRPC1 ion channel in hippocampal neurons. Front. Neurosci. Conference Abstract: 12th National Congress of the Belgian Society for Neuroscience. doi: 10.3389/conf.fnins.2017.94.00031 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: 29 Apr 2017; Published Online: 25 Jan 2019. * Correspondence: Mrs. Sophie Lepannetier, Université catholique de Louvain, Institute of Neuroscience, Brussels, 1150, Belgium, slepannetier@gmail.com 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 Sophie Lepannetier Olivier Schakman Francois Seghers Philippe Gailly Google Sophie Lepannetier Olivier Schakman Francois Seghers Philippe Gailly Google Scholar Sophie Lepannetier Olivier Schakman Francois Seghers Philippe Gailly PubMed Sophie Lepannetier Olivier Schakman Francois Seghers Philippe Gailly Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.