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Patients with RA rate pain relief as the highest priority; however, few studies have addressed the efficacy and safety of therapies directed specifically toward pain pathways. The \u03c9\u2010conotoxin MVIIA (ziconotide) is used in humans to alleviate persistent pain syndromes, because it specifically blocks the voltage\u2010gated calcium 2.2 (Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.2) channel, which mediates the release of neurotransmitters and proinflammatory mediators from peripheral nociceptor nerve terminals. The aims of this study were to investigate whether blockade of Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.2 can suppress arthritis pain, and to examine the progression of induced arthritis during persistent Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.2 blockade.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Transgenic mice expressing a membrane\u2010tethered form of MVIIA under the control of a nociceptor\u2010specific gene (MVIIA\u2010transgenic mice) were used in the experiments. The mice were subjected to unilateral induction of joint inflammation using a combination of antigen and collagen.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.2 blockade mediated by tethered MVIIA effectively suppressed arthritis\u2010induced pain; however, in contrast to their wild\u2010type littermates, which ultimately regained use of their injured joint as inflammation subsided, MVIIA\u2010transgenic mice showed continued inflammation, with up\u2010regulation of the osteoclast activator RANKL and concomitant joint and bone destruction.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Taken together, our results indicate that alleviation of peripheral pain by blockade of Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.2\u2010 mediated calcium influx and signaling in nociceptor sensory neurons impairs recovery from induced arthritis and point to the potentially devastating effects of using Ca\n                      <jats:sub>V<\/jats:sub>\n                      2.2 channel blockers as analgesics during inflammation.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.39094","type":"journal-article","created":{"date-parts":[[2015,3,2]],"date-time":"2015-03-02T10:51:19Z","timestamp":1425293479000},"page":"1657-1667","source":"Crossref","is-referenced-by-count":11,"title":["Suppression of Peripheral Pain by Blockade of Voltage\u2010Gated Calcium 2.2 Channels in Nociceptors Induces RANKL and Impairs Recovery From Inflammatory Arthritis in a Mouse Model"],"prefix":"10.1002","volume":"67","author":[{"given":"Uta","family":"Baddack","sequence":"first","affiliation":[{"name":"Max Delbr\u00fcck Centre for Molecular Medicine Berlin Germany and Centre National de la Recherche Scientifique Toulouse France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silke","family":"Frahm","sequence":"additional","affiliation":[{"name":"Charit\u00e9\u2013Universit\u00e4tsmedizin Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beatriz","family":"Antolin\u2010Fontes","sequence":"additional","affiliation":[{"name":"The Rockefeller University New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jenny","family":"Grobe","sequence":"additional","affiliation":[{"name":"Max Delbr\u00fcck Centre for Molecular Medicine Berlin Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Martin","family":"Lipp","sequence":"additional","affiliation":[{"name":"Max 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