Extrasynaptic GABAergic currents in hippocampus are inhibited by adenosine A1 receptors

Abstract

Event Abstract Back to Event Extrasynaptic GABAergic currents in hippocampus are inhibited by adenosine A1 receptors R. Dias1, J. Ribeiro1, D. Rombo1* and A. Sebastião1 1 Instituto de Farmacologia e Neurociências, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Portugal Adenosine, through inhibitory A1 receptors is a modulator of neuronal excitability in the hippocampus by modulating the glutamatergic excitatory circuit at the pre- and postsynaptic level. The role of adenosine on GABAergic transmission in the hippocampus is much less known. We now investigated whether adenosine, through A1 receptors, modulates postsynaptic currents mediated by GABAA receptors. Muscimol (30µM, GABAA receptor agonist)-evoked postsynaptic currents (PSCs), afferent-evoked inhibitory postsynaptic currents (IPSCs) and miniature inhibitory postsynaptic currents (mIPSCs), were recorded (whole-cell configuration, Vh=-80mV) from CA1 pyramidal cells and interneurons of rat (Wistar, 3-5w) hippocampal slices. At CA1 pyramidal cells, the activation of A1 receptors with CPA (10-30nM) decreased (to 54±3.9%,p<0.0001,n=12) the peak amplitude of PSCs and this inhibition was reversed by DPCPX (50nM), an adenosine A1 receptor antagonist, to 83±2.5% of baseline (n=4,p<0.05). DPCPX per se unmasked the inhibition of PSCs by endogenous extracellular adenosine since it increased the inhibitory currents by 13±1.0% (n=5,p<0.001). Neither the amplitude nor the frequency of mIPSCs (n=12), or the amplitude of IPSCs (n=10), were affected by CPA indicating an action of A1 receptors on extrasynaptic GABAergic currents. At stratum radiatum GABAergic interneurons, the activation of A1 receptors with CPA attenuated GABAA PSCs in 4 out of 9 cells tested to 57±2.3% (p<0.001). The PSCs in the other 5 cells tested were not changed by CPA superfusion, suggesting the existence of two populations of interneurons differently sensitive to adenosine. Together, these results indicate that extrasynaptic GABAA receptor-mediated currents are modulated by adenosine A1 receptors in pyramidal hippocampal neurons and in a subset of interneurons. Support:FCT Conference: EMBO workshop: Gaba Signalling and Brain Networks , Amsterdam, Netherlands, 30 Jun - 2 Jul, 2010. Presentation Type: Poster Presentation Topic: Posters Citation: Dias R, Ribeiro J, Rombo D and Sebastião A (2010). Extrasynaptic GABAergic currents in hippocampus are inhibited by adenosine A1 receptors. Conference Abstract: EMBO workshop: Gaba Signalling and Brain Networks . doi: 10.3389/conf.fnins.2010.15.00021 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: 24 Jun 2010; Published Online: 24 Jun 2010. * Correspondence: D. Rombo, Instituto de Farmacologia e Neurociências, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal, drombo@fm.ul.pt 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 R. Dias J. Ribeiro D. Rombo A. Sebastião Google R. Dias J. Ribeiro D. Rombo A. Sebastião Google Scholar R. Dias J. Ribeiro D. Rombo A. Sebastião PubMed R. Dias J. Ribeiro D. Rombo A. Sebastião 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.