Event Abstract Back to Event In Vivo inactivation of nitric oxide in the rat CNS:Quantitative and mechanistic features Ricardo M. Santos1*, Catia F. Lourenco1, Greg A. Gerhardt2, Joao Laranjinha1, 3 and Rui M. Barbosa1, 3 1 University of Coimbra, Center for Neuroscience and Cell Biology, Portugal 2 University of Kentucky, Center for Microelectrode Technology, United States 3 University of Coimbra, Faculty of Pharmacy, Portugal Nitric oxide (NO) is a ubiquitous free radical neuromodulator that conveys information associated with its concentration dynamics in brain tissue. The regulation of its enzymatic production is strongly substantiated but, conversely, the lack of studies regarding NO inactivation in vivo in the brain, largely due to the difficulty of its direct measurement at low concentrations with high temporal resolution, has prevented the elucidation of its neuromodulatory role on mechanistic and quantitative basis. In this study, we experimentally addressed the kinetics of NO inactivation in vivo in the rat brain cortex and hippocampal CA1 region by measuring locally applied NO with home-made NO selective carbon fiber microelectrodes stereotaxically inserted into the selected brain regions.We found that NO is strongly inactivated in the rat brain in vivo, with apparent first order kinetics, for NO concentrations below 2 μM. Apparent first order decay rate constants (k) of NO signals decreased in a sigmoid fashion with increasing NO concentrations in vivo from 0.93 to 0.51 s-1 (EC50 = 16.6 μM) and from 1.05 to 0.57 s-1 (EC50 = 3.2 μM) in the cortex and hippocampus, respectively, suggesting distinct ability of these brain regions to inactivate NO. Based on mathematical modeling of NO signals, we estimate that, below 2 μM, inactivation reactions impose an NO half-life of 0.75 s in the cortex and 0.56 s in the hippocampus.After inducing global ischemia, NO signals amplitude increased and k values decreased to diffusion values (similar to those in agarose gel used as control for NO diffusion). These observations together with our kinetic results suggest a non-saturable mechanism of NO removal and blood flow as determinant for brain ability to inactivate NO in vivo. Moreover, preliminary experiments, concerning the simultaneous measurement of NO and oxygen tension in the brain in vivo, suggest that NO inactivation is largely independent of oxygen tension. Based on our results, we propose hemoglobin as a major contributor for the observed NO decay in vivo in the brain. Conference: 11th Meeting of the Portuguese Society for Neuroscience, Braga, Portugal, 4 Jun - 6 Jun, 2009. Presentation Type: Poster Presentation Topic: Neuronal Communication Citation: Santos RM, Lourenco CF, Gerhardt GA, Laranjinha J and Barbosa RM (2009). In Vivo inactivation of nitric oxide in the rat CNS:Quantitative and mechanistic features. Front. Neurosci. Conference Abstract: 11th Meeting of the Portuguese Society for Neuroscience. doi: 10.3389/conf.neuro.01.2009.11.127 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: 11 Aug 2009; Published Online: 11 Aug 2009. * Correspondence: Ricardo M Santos, University of Coimbra, Center for Neuroscience and Cell Biology, Alicante, Portugal, ricardo_dos_santos@hotmail.com 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 Ricardo M Santos Catia F Lourenco Greg A Gerhardt Joao Laranjinha Rui M Barbosa Google Ricardo M Santos Catia F Lourenco Greg A Gerhardt Joao Laranjinha Rui M Barbosa Google Scholar Ricardo M Santos Catia F Lourenco Greg A Gerhardt Joao Laranjinha Rui M Barbosa PubMed Ricardo M Santos Catia F Lourenco Greg A Gerhardt Joao Laranjinha Rui M Barbosa 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.