{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,5]],"date-time":"2026-10-05T07:01:58Z","timestamp":1791183718750,"version":"4.1.0"},"reference-count":74,"publisher":"SAGE Publications","issue":"1","license":[{"start":{"date-parts":[[2014,5,12]],"date-time":"2014-05-12T00:00:00Z","timestamp":1399852800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Cephalalgia"],"published-print":{"date-parts":[[2015,1]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Trigeminal neuralgia is a disorder of paroxysmal and severely disabling facial pain and continues to be a real therapeutic challenge. At present there are few effective drugs. Here the aim of this study was to investigate the role of BK\n                      <jats:sub>Ca<\/jats:sub>\n                      channels in trigeminal neuropathic pain.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Rats were divided into two groups: a sham and a chronic constriction injury of infraorbital branch of trigeminal nerve (ION-CCI) group. Nociceptive behavior testing, immunohistochemistry, RT-PCR, Western blotting and whole-cell patch clamp recording were used.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Relative to the sham group, rats with ION-CCI consistently displayed lower mechanical pain thresholds in the vibrissal pad region from day 6 to 42 after ION-CCI operation. ION-CCI induced a significant down-regulation of BK\n                      <jats:sub>Ca<\/jats:sub>\n                      channels both in mRNA and protein levels in the ipsilateral trigeminal ganglion (TG), a lower threshold intensity of action potential, and decreased total BK\n                      <jats:sub>Ca<\/jats:sub>\n                      currents in cultured TG neurons. TG target injection of NS1619 (20\u2013100\u2009\u00b5g), an opener of BK\n                      <jats:sub>Ca<\/jats:sub>\n                      channels, dose-dependently increased the mechanical pain threshold, which was blocked by the BK\n                      <jats:sub>Ca<\/jats:sub>\n                      channel inhibitor iberiotoxin (IbTX, 20\u2009\u00b5g). NS1619 (10\u2009\u00b5M) significantly increased the mean threshold intensities of action potentials in ION-CCI rats, while failing to affect those in the sham rats. The levels of phosphorylated extracellular signal-regulated kinase (ERK), p38 and c-Jun N-terminal kinases (JNK) in TG were significantly increased after ION-CCI operation. The ERK1\/2 antagonist U0126, p38 antagonist SB203580 and JNK antagonist SP600125 significantly reversed the facial mechanical allodynia in ION-CCI rats. However, the ERK1\/2 antagonist U0126, p38 antagonist SB203580 but not JNK antagonist SP600125 significantly increased BK\n                      <jats:sub>Ca<\/jats:sub>\n                      currents in ION-CCI TG neurons.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our results indicate the important involvement of mainly ERK and p38 MAPK pathways in modulating BK\n                      <jats:sub>Ca<\/jats:sub>\n                      channels in ION-CCI TG neurons. BK\n                      <jats:sub>Ca<\/jats:sub>\n                      channels represent a new therapeutic target for the clinical treatment of trigeminal neuropathic pain.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/0333102414534083","type":"journal-article","created":{"date-parts":[[2014,5,13]],"date-time":"2014-05-13T02:50:41Z","timestamp":1399949441000},"page":"16-35","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":45,"title":["The role of large-conductance, calcium-activated potassium channels in a rat model of trigeminal neuropathic pain"],"prefix":"10.1177","volume":"35","author":[{"given":"Cai-Yue","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Physiology and Key Laboratory of Molecular Neurobiology, Ministry of Education, Second Military Medical University, PR China"},{"name":"Department of Stomatology, Changzheng Hospital, Second Military 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