Vicente García, Rubén, 1978-Coma Camprodón, MireiaBusquets, SilviaMoore Carrasco, RodrigoLópez Soriano, Francisco J.Argilés, Josep M.Felipe, Antonio2016-01-202016-01-202004Vicente R, Coma M, Busquets S, Moore-Carrasco R, López-Soriano FJ, Argilés JM et al. The systemic inflammatory response is involved in the regulation of K(+) channel expression in brain via TNF-alpha-dependent and -independent pathways. FEBS Letters. 2004;572(1-3):189-94. DOI: 10.1016/j.febslet.2004.07.0300014-5793http://hdl.handle.net/10230/25610TNF-alpha, generated during the systemic inflammatory response, triggers a wide range of biological activities that mediate the neurologic manifestations associated with cancer and infection. Since this cytokine regulates ion channels in vitro (especially Kv1.3 and Kir2.1), we aimed to study Kv1.3 and Kir2.1 expression in brain in response to in vivo systemic inflammation. Cancer-induced cachexia and LPS administration increased plasma TNF-alpha. Kv1.3 and Kir2.1 expression was impaired in brain during cancer cachexia. However, LPS treatment induced Kv1.3 and downregulated Kir2.1 expression, and TNF-alpha administration mimicked these results. Experiments using TNF-alpha double receptor knockout mice demonstrated that the systemic inflammatory response mediates K(+) channel regulation in brain via TNF-alpha-dependent and -independent redundant pathways. In summary, distinct neurological alterations associated with systemic inflammation may result from the interaction of various cytokine pathways tuning ion channel expression in response to neurophysiological and neuroimmunological processes.application/pdfeng© Elsevier. This is the published version of an article http://dx.doi.org/10.1016/j.febslet.2004.07.030 that appeared in the journal FEBS Letters. It is published in an Open Archive under an Elsevier user license. Details of this licence are available here: http://www.elsevier.com/about/open-access/open-access-policies/oa-license-policy/elsevier-user-licenseCanals de potassiInflamacióinfo:eu-repo/semantics/articlehttp://dx.doi.org/10.1016/j.febslet.2004.07.030Kþ channelsCancer cachexiaSystemic inflammatory responseBrainTNF-aLipopolysaccharideinfo:eu-repo/semantics/openAccess