Abstract
Event Abstract Back to Event Postsynaptic Group II Metabotropic Glutamate Receptor activation in Dentate Gyrus Granule Cells J. Brunner1*, T. Andrási1, S. Van-Weert1, F. K. Borgmann2, S. Jessberger2 and J. Szabadics1 1 Hungarian Academy of Sciences, Institute of Experimental Medicine, Hungary 2 Swiss Federal Institute of Technology, Institute of Cell Biology, Switzerland Dentate gyrus granule cells (DGGCs) express group II metabotropic glutamate receptors (mGluR2/3) both on their axonal and somatodendritic membranes. Activation of axonal mGluR2/3s suppress the synaptic transmission from DGGCs due to down regulation of presynaptic Ca2+ channel activity. However, the function of dendritic mGluR2/3s in DGGCs is not known. First, we showed that bath application of mGluR2/3 selective agonists (DCG IV, APDC) resulted in significant, long-lasting hyperpolarization in DGGCs and this effect persisted in the presence of TTX but it was prevented by selective antagonists (APICA, LY 341495). DCG IV did not have any effect on the axonal membrane potential of DGGCs indicating distinct somatic and axonal mGluR2/3 mediated mechanisms. The hyperpolarizing DCG IV effect was absent in GABAergic and CA3 pyramidal cells. We also showed that the mGluR2/3 activation induced somatodendritic hyperpolarization was mediated by GIRK channels as intracellular GDPβS and bath application of inward-rectifier potassium channel blocker, tertiapin-Q occluded the DCG IV effect. Lastly, focal glutamate release by photolysis of MNI-glutamate in the perisomatic region of DGGCs resulted in mGluR2/3 mediated currents; however, similar current could be evoked in the dendritic region (>15 µm) suggesting that mGluR2/3 are activated by a specific glutamatergic source which innervates the perisomatic region of DGGCs and elicit mGluR2/3 mediated glutamatergic inhibition. Keywords: Neurophysiology, Neuroscience Conference: 13th Conference of the Hungarian Neuroscience Society (MITT), Budapest, Hungary, 20 Jan - 22 Jan, 2011. Presentation Type: Abstract Topic: Neurophysiology Citation: Brunner J, Andrási T, Van-Weert S, Borgmann FK, Jessberger S and Szabadics J (2011). Postsynaptic Group II Metabotropic Glutamate Receptor activation in Dentate Gyrus Granule Cells. Front. Neurosci. Conference Abstract: 13th Conference of the Hungarian Neuroscience Society (MITT). doi: 10.3389/conf.fnins.2011.84.00100 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: 03 Mar 2011; Published Online: 23 Mar 2011. * Correspondence: Dr. J. Brunner, Hungarian Academy of Sciences, Institute of Experimental Medicine, Budapest, Hungary, brunner.janos@koki.hu 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 J. Brunner T. Andrási S. Van-Weert F. K Borgmann S. Jessberger J. Szabadics Google J. Brunner T. Andrási S. Van-Weert F. K Borgmann S. Jessberger J. Szabadics Google Scholar J. Brunner T. Andrási S. Van-Weert F. K Borgmann S. Jessberger J. Szabadics PubMed J. Brunner T. Andrási S. Van-Weert F. K Borgmann S. Jessberger J. Szabadics 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.
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