Characterization of K+ depolarization evoked ATP, adenosine and glutamate release in rat hippocampus: a microelectrode biosensor study

Abstract

Event Abstract Back to Event Characterization of K+ depolarization evoked ATP, adenosine and glutamate release in rat hippocampus: a microelectrode biosensor study Attila Heinrich1* and Beáta Sperlágh1 1 Institute of Experimental Medicine, Hungarian Academy of Sciences, Laboratory of Molecular Pharmacology, Hungary Glial cells are active players in information processing in the brain and both adenine nucleotides and nucleosides as well as glutamate play a key role in glia-neuron interactions. These 'gliotransmitters' signal either to astrocytes, where they generate Ca2+ waves, or to neurons, where they modulate synaptic transmission and neuronal excitability. However, the physiological trigger for the release of ATP from astrocytes and its mechanism is still unknown. In our study rat hippocampal slices were depolarized with 25 mM K+ and the release of ATP, adenosine and glutamate were recorded with enzymatic microelectrode biosensors. ATP and glutamate sensor exhibited a rapidly increasing current during K+ depolarization. In the presence of ARL67156 the extracellular level of ATP was encanced and the detected long lasting adenosine efflux was totally inhibited suggesting that generation of adenosine may arise from the extracellular breakdown of ATP. Ca2+-free medium abolished both ATP and adenosine release in response to K+ depolarization. ATP, adenosine and glutamate release was reduced in the presence of the Na+-channel blocker, TTX. Extracellular accumulation of ATP and adenosine were significantly decreased in the presence of NMDA receptor antagonist D-AP-5. High concentration of carbenoxolone, totally inhibited the ATP, adenosine and glutamate efflux, while in pannexin-selective low concentration CBX decreased only the adenosine efflux. Perfusion with the glia-selective toxin fluoroacetate significantly inhibited concentration of ATP, adenosine and glutamate. Our results demonstrate that ATP and adenosine release are mediated by axonal activation via NMDA receptors and probably derived from glial cells through different gap junction hemichannels. Although the efflux of adenosine did arise from previously released ATP, it is also released directly via pannexin hemichannels. ATP is released through gap junction hemichannel into extracellular space, before it is rapid breakdown to adenosine. Conference: IBRO International Workshop 2010, Pécs, Hungary, 21 Jan - 23 Jan, 2010. Presentation Type: Poster Presentation Topic: Cellular neuroscience Citation: Heinrich A and Sperlágh B (2010). Characterization of K+ depolarization evoked ATP, adenosine and glutamate release in rat hippocampus: a microelectrode biosensor study. Front. Neurosci. Conference Abstract: IBRO International Workshop 2010. doi: 10.3389/conf.fnins.2010.10.00046 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: 20 Apr 2010; Published Online: 20 Apr 2010. * Correspondence: Attila Heinrich, Institute of Experimental Medicine, Hungarian Academy of Sciences, Laboratory of Molecular Pharmacology, Budapest, Hungary, heinrich@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 Attila Heinrich Beáta Sperlágh Google Attila Heinrich Beáta Sperlágh Google Scholar Attila Heinrich Beáta Sperlágh PubMed Attila Heinrich Beáta Sperlágh 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.