Event Abstract Back to Event NMDA Receptor Mediated Dendritic Spikes in CA1 Stratum Radiatum Interneurons Gergely Turi1*, Attila Kaszas1, Gergely Katona1, Balazs Chiovini1, Vizi E. Szilveszter1 and Balazs Rozsa1 1 Institute of Experimental Medicine, Hungarian Academy of Sciences, Hungary Although the anatomical properties of glutamatergic synapses on dendrites of hippocampal interneurons are well characterized, the source and pharmacological property of calcium transients as a consequence of the glutamatergic neurotransmission remain to be clarified. In order to study the pharmacology of the calcium transients evoked by excitatory synaptic transmission in the dendrites of CA1 hippocampal interneurons, two-photon imaging was used in combination with focal synaptic stimulation and rapid drug application. Our data revealed that local administration of AP5, an NMDA receptor antagonist could significantly attenuate the amplitude of both locally evoked calcium transients and EPSPs in the distal dendritic segments of interneurons. The role of NMDA receptors as the main source of calcium influx was further supported by whole-cell recordings performed in Mg-free ACSF that resulted in robust elevation of synaptic calcium influx and amplitude of EPSPs. Moreover, increasing stimulation for excitatory inputs evoked local dendritic spikes (dSpikes) that could be described with larger peak amplitude of the calcium transients paired with a larger amplitude and slower decay of EPSPs. The dSpikes could not be detected when AP5 was administered locally. These results indicate that in the dendrites of CA1 interneurons NMDA receptors might serve as the main source of glutamatergic neurotransmission evoked calcium influx. Furthermore, focal synaptic stimulation is able to evoke dSpikes, which are also NMDA receptor dependent. The dSpikes described in our experiments may have a key role in dendritic signal integration. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Research on the cerebral cortex and related structures Citation: Turi G, Kaszas A, Katona G, Chiovini B, Szilveszter VE and Rozsa B (2009). NMDA Receptor Mediated Dendritic Spikes in CA1 Stratum Radiatum Interneurons. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.224 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: 09 Mar 2009; Published Online: 09 Mar 2009. * Correspondence: Gergely Turi, Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest, Hungary, turig@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 Gergely Turi Attila Kaszas Gergely Katona Balazs Chiovini Vizi E Szilveszter Balazs Rozsa Google Gergely Turi Attila Kaszas Gergely Katona Balazs Chiovini Vizi E Szilveszter Balazs Rozsa Google Scholar Gergely Turi Attila Kaszas Gergely Katona Balazs Chiovini Vizi E Szilveszter Balazs Rozsa PubMed Gergely Turi Attila Kaszas Gergely Katona Balazs Chiovini Vizi E Szilveszter Balazs Rozsa 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.