Over-expression of HCN2 ion channels in the superficial spinal dorsal horn of rats in Freund’s adjuvant-induced inflammatory pain

Abstract

Event Abstract Back to Event Over-expression of HCN2 ion channels in the superficial spinal dorsal horn of rats in Freund’s adjuvant-induced inflammatory pain Ildikó Papp1*, Krisztina Holló1, Krisztina Hegedus1 and Miklos Antal1 1 Department of Anatomy, MHSC, University of Debrecen, Hungary We have recently demonstrated that hyperpolarization-activated and cyclic nucleotide-gated cation channel subunit 2 (HCN2) is widely expressed by axon terminals of substance P-containing (SP) peptidergic nociceptive primary afferents in laminae I-IIo of the spinal dorsal horn. In the present study, we investigated how this expression pattern of HCN2 ion channels is changed by complete Freund’s adjuvant (CFA)-induced inflammation of the hindpaw. We found that three days after CFA injection, when the nociceptive responsiveness of the inflamed hindpaw and c-Fos immunoreactivity of the spinal dorsal horn substantially increased, the numbers of HCN2 immunolabeled axon terminals were also significantly augmented in laminae I-IIo at the L4 segment of the spinal dorsal horn ipsilateral to the site of CFA injection. The elevation of HCN2 immunoreactivity was paralleled with the increase in SP immunoreactivity. In addition, in sections double-stained for SP and HCN2 we found that, similarly to control animals, the co-localization between HCN2 and SP immunoreactivity was remarkably high, suggesting that nociceptive primary afferents that increased their SP expression in response to CFA injection into the hindpaw also increased their HCN2 expression. Interestingly enough, while SP expression remained unchanged, HCN2 expression substantially increased also in laminae I-IIo of the spinal dorsal horn contralateral to the site of CFA injection. The results indicate that HCN2 ion channel mechanisms may have some role in the development of central sensitization of spinal pain processing neural circuits in chronic inflammatory pain conditions. Conference: 12th Meeting of the Hungarian Neuroscience Society, Budapest, Hungary, 22 Jan - 24 Jan, 2009. Presentation Type: Poster Presentation Topic: Pathophysiology and neurology - non-degenerative disorders Citation: Papp I, Holló K, Hegedus K and Antal M (2009). Over-expression of HCN2 ion channels in the superficial spinal dorsal horn of rats in Freund’s adjuvant-induced inflammatory pain. Front. Syst. Neurosci. Conference Abstract: 12th Meeting of the Hungarian Neuroscience Society. doi: 10.3389/conf.neuro.01.2009.04.037 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: Ildikó Papp, Department of Anatomy, MHSC, University of Debrecen, Debrecen, Hungary, pildiko@chondron.anat.dote.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 Ildikó Papp Krisztina Holló Krisztina Hegedus Miklos Antal Google Ildikó Papp Krisztina Holló Krisztina Hegedus Miklos Antal Google Scholar Ildikó Papp Krisztina Holló Krisztina Hegedus Miklos Antal PubMed Ildikó Papp Krisztina Holló Krisztina Hegedus Miklos Antal 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.