| Literature DB >> 20100565 |
Ana Ledo1, Rui Barbosa, Enrique Cadenas, João Laranjinha.
Abstract
Nitric oxide (*NO) is a ubiquitous signaling molecule that participates in the neuromolecular phenomena associated with memory formation. In the hippocampus, neuronal *NO production is coupled to the activation of the NMDA-type of glutamate receptor. Although *NO-mediated signaling has been associated with soluble guanylate cyclase activation, cytochrome oxidase is also a target for this gaseous free radical, for which *NO competes with O(2). Here we show, for the first time in a model preserving tissue cytoarchitecture (rat hippocampal slices) and at a physiological O(2) concentration, that endogenous NMDA-evoked *NO production inhibits tissue O(2) consumption for submicromolar concentrations. The simultaneous real-time recordings reveal a direct correlation between the profiles of *NO and O(2) in the CA1 subregion of the hippocampal slice. These results, obtained in a system close to in vivo models, strongly support the current paradigm for O(2) and *NO interplay in the regulation of cellular respiration. Copyright 2010 Elsevier Inc. All rights reserved.Entities:
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Year: 2010 PMID: 20100565 PMCID: PMC2839026 DOI: 10.1016/j.freeradbiomed.2010.01.024
Source DB: PubMed Journal: Free Radic Biol Med ISSN: 0891-5849 Impact factor: 7.376