Event Abstract Back to Event Modulation of INaP mediated bursting in trigeminal main sensory neurons by Ca++ and synaptic inputs Arlette Kolta1* 1 Université de Montréal, Departement de Stomatologie, Canada It is generally admitted that all repetitive movements are governed by central pattern generators. These are networks able to produce rhythmic movements that while being stereotyped, are still adapted and can vary from cycle to cycle in function of sensory information. Studies at the cellular level have focused on the mechanisms responsible for rhythmogenesis in these networks, but little has examined those allowing for adaption and variability of their rhythmic outputs. This will be precisely the topic of this symposium where speakers will present mechanisms used by different CPGs to generate and modulate their rhythmic output in different conditions. In most of these mechanisms, Ca++ is a key player. In the masticatory system that is governed by trigeminal circuits and more precisely the main sensory nucleus (NVsnpr), rhythmogenesis relies on a sodium persistent current (INap) which is inversely modulated by the extracellular concentration of Ca++ ([Ca++] e) so that a decrease in [Ca++] e causes an increase in the probability of activating INaP and bursting. We propose that through this mechanism incoming inputs (from sensory or cortical fibres) can trigger bursting and adjust its frequency to the appropriate level by causing a decrease of [Ca++] e. In this model, we propose that glia plays an important role by responding to neuronal activity from the incoming inputs and by regulating the level of [Ca++] e in return. In support of this model, we have shown that repetitive activation of sensory fibers projecting to NVsnpr causes rhythmic bursting in about 30 % of its neurons, synchronization of multiple units and increases coupling between glial cells within the nucleus. NMDA, but not AMPA mimic the effect of stimulation of the sensory tract on both bursting and glial cells coupling and their blockade prevents stimulation-induced bursting. Gap junctions blockers disrupt NMDA induced bursting and we assume that this effect is achieved by an action on glial gap junctions since very little coupling (if any) exists between neurons in this nucleus. These studies will deepen our understanding of the potential role of neuron-glia interactions in rhythmic activities of the brain. Conference: 3rd Mediterranean Conference of Neuroscience , Alexandria, Egypt, 13 Dec - 16 Dec, 2009. Presentation Type: Oral Presentation Topic: Symposium 05 – Interactions of synaptic and intrinsic properties in rhythmic motor activities Citation: Kolta A (2009). Modulation of INaP mediated bursting in trigeminal main sensory neurons by Ca++ and synaptic inputs. Front. Neurosci. Conference Abstract: 3rd Mediterranean Conference of Neuroscience . doi: 10.3389/conf.neuro.01.2009.16.024 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: 19 Nov 2009; Published Online: 19 Nov 2009. * Correspondence: Arlette Kolta, Université de Montréal, Departement de Stomatologie, Beauport, Qc G1J 2G3, Canada, arlette.kolta@umontreal.ca 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 Arlette Kolta Google Arlette Kolta Google Scholar Arlette Kolta PubMed Arlette Kolta 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.