{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T18:51:24Z","timestamp":1791917484365,"version":"4.3.4"},"reference-count":35,"publisher":"Wiley","license":[{"start":{"date-parts":[[2013,1,1]],"date-time":"2013-01-01T00:00:00Z","timestamp":1356998400000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AG038778"],"award-info":[{"award-number":["AG038778"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AR055104"],"award-info":[{"award-number":["AR055104"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AG038778"],"award-info":[{"award-number":["AG038778"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["AR055104"],"award-info":[{"award-number":["AR055104"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["BioMed Research International"],"published-print":{"date-parts":[[2013]]},"abstract":"<jats:p>Malignant hyperthermia (MH) is a pharmacogenetic disorder most often linked to mutations in the type 1 ryanodine receptor (RyR1) or the skeletal L-type Ca<jats:sup>2+<\/jats:sup>channel (Ca<jats:sub>V<\/jats:sub>1.1). The only effective treatment for an MH crisis is administration of the hydantoin derivative Dantrolene. In addition to reducing voltage induced Ca<jats:sup>2+<\/jats:sup>release from the sarcoplasmic reticulum, Dantrolene was recently found to inhibit L-type currents in developing myotubes by shifting the voltage-dependence of Ca<jats:sub>V<\/jats:sub>1.1 channel activation to more depolarizing potentials. Thus, the purpose of this study was to obtain information regarding the mechanism of Dantrolene-induced inhibition of Ca<jats:sub>V<\/jats:sub>1.1. A mechanism involving a general depression of plasma membrane excitability was excluded because the biophysical properties of skeletal muscle Na<jats:sup>+<\/jats:sup>current in normal mouse myotubes were largely unaffected by exposure to Dantrolene. However, a role for RyR1 was evident as Dantrolene failed to alter the amplitude, voltage dependence and inactivation kinetics of L-type currents recorded from<jats:italic>dyspedic<\/jats:italic>(RyR1 null) myotubes. Taken together, these results suggest that the mechanism of Dantrolene-induced inhibition of the skeletal muscle L-type Ca<jats:sup>2+<\/jats:sup>current is related to altered communication between Ca<jats:sub>V<\/jats:sub>1.1 and RyR1.<\/jats:p>","DOI":"10.1155\/2013\/390493","type":"journal-article","created":{"date-parts":[[2012,12,5]],"date-time":"2012-12-05T23:54:55Z","timestamp":1354751695000},"page":"1-10","source":"Crossref","is-referenced-by-count":22,"title":["Dantrolene-Induced Inhibition of Skeletal L-Type Ca<sup>2+<\/sup>Current Requires RyR1 Expression"],"prefix":"10.1155","volume":"2013","author":[{"given":"R. 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