A Glycinergic input into the intralaminar thalamic nuclei

Abstract

Event Abstract Back to Event A Glycinergic input into the intralaminar thalamic nuclei Kristof Giber1*, Viktor Plattner1, Hajnalka Bokor1 and Laszlo Acsady1 1 Dept. Cellular and Network Neurobiology , Institute of Experimental Medicine, Hungary In humans intralaminar thalamus is critical to maintain normal conscious states. Recently these nuclei were shown to receive a selective and dense glycinergic input in transgenic mice expressing EGFP linked to the glycine-transporter-2 protein (GlyT2). The aims of the present study were to determine the origin of the Glyt2-positive thalamic fibers, to characterize the morphology and co-transmitter of the glycinergic axon terminals and to examine the firing properties of the projecting neurons in vivo. Following the injections of retrograde tracer fluorogold into the intralaminar thalamus, the largest proportion (51.5%) of the labeled glycinergic neurons were localized within the the ipsilateral oral and caudal pontine nuclei (PnO-PnC). Sixty-one percent of the projecting cells in this region were EGFP-positive, whereas most contralateral neurons were GlyT2-negative. Injections of anterograde tracer Phaseolus vulgaris leucoagglutine into the PnO-PnC resulted in a dense labeling of large terminals in the ipsilateral intralaminar nuclei. Out of these terminals, 48.9% were EGFP-positive, while this ratio was only 9.6% in the contralateral hemisphere. The GlyT2-positive boutons were GABA-immunopositive and established multiple synapses on the proximal dendrites of relay cells. Juxtacellular recording of a GlyT2-positive PnO cell projecting to the thalamus disclosed a firing pattern consisting of rhythmic clusters of spikes at 40-50Hz in synchrony with the EEG upstates. We demonstrated that beside the well-known excitatory ascending activating system a novel inhibitory pathway reaches the thalamus from the brainstem. The glycine- and GABAergic ponto-thalamic pathway raises the question how an inhibitory arousal system modulates the thalamic activity and the conscious states. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Developmental neurobiology and subcortical functions Citation: Giber K, Plattner V, Bokor H and Acsady L (2009). A Glycinergic input into the intralaminar thalamic nuclei. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.056 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: 27 Feb 2009; Published Online: 27 Feb 2009. * Correspondence: Kristof Giber, Dept. Cellular and Network Neurobiology , Institute of Experimental Medicine, Budapest, Hungary, giber@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 Kristof Giber Viktor Plattner Hajnalka Bokor Laszlo Acsady Google Kristof Giber Viktor Plattner Hajnalka Bokor Laszlo Acsady Google Scholar Kristof Giber Viktor Plattner Hajnalka Bokor Laszlo Acsady PubMed Kristof Giber Viktor Plattner Hajnalka Bokor Laszlo Acsady 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.