{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T13:41:17Z","timestamp":1789911677134,"version":"4.0.1"},"reference-count":126,"publisher":"Rockefeller University Press","issue":"5","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2014,11,1]]},"abstract":"<jats:p>Huntington\u2019s disease (HD) is caused by an expanded CAG trinucleotide repeat within the gene encoding the protein huntingtin. The resulting elongated glutamine (poly-Q) sequence of mutant huntingtin (mhtt) affects both central neurons and skeletal muscle. Recent reports suggest that ryanodine receptor\u2013based Ca2+ signaling, which is crucial for skeletal muscle excitation\u2013contraction coupling (ECC), is changed by mhtt in HD neurons. Consequently, we searched for alterations of ECC in muscle fibers of the R6\/2 mouse, a mouse model of HD. We performed fluorometric recordings of action potentials (APs) and cellular Ca2+ transients on intact isolated toe muscle fibers (musculi interossei), and measured L-type Ca2+ inward currents on internally dialyzed fibers under voltage-clamp conditions. Both APs and AP-triggered Ca2+ transients showed slower kinetics in R6\/2 fibers than in fibers from wild-type mice. Ca2+ removal from the myoplasm and Ca2+ release flux from the sarcoplasmic reticulum were characterized using a Ca2+ binding and transport model, which indicated a significant reduction in slow Ca2+ removal activity and Ca2+ release flux both after APs and under voltage-clamp conditions. In addition, the voltage-clamp experiments showed a highly significant decrease in L-type Ca2+ channel conductance. These results indicate profound changes of Ca2+ turnover in skeletal muscle of R6\/2 mice and suggest that these changes may be associated with muscle pathology in HD.<\/jats:p>","DOI":"10.1085\/jgp.201411255","type":"journal-article","created":{"date-parts":[[2014,10,27]],"date-time":"2014-10-27T15:16:07Z","timestamp":1414422967000},"page":"393-413","update-policy":"https:\/\/doi.org\/10.1085\/jgp.crossmarkpolicy","source":"Crossref","is-referenced-by-count":30,"title":["Altered Ca2+ signaling in skeletal muscle fibers of the R6\/2 mouse, a model of Huntington\u2019s disease"],"prefix":"10.1085","volume":"144","author":[{"given":"Peter","family":"Braubach","sequence":"first","affiliation":[{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Murat","family":"Orynbayev","sequence":"additional","affiliation":[{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zoita","family":"Andronache","sequence":"additional","affiliation":[{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tanja","family":"Hering","sequence":"additional","affiliation":[{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"},{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Georg Bernhard","family":"Landwehrmeyer","sequence":"additional","affiliation":[{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katrin S.","family":"Lindenberg","sequence":"additional","affiliation":[{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Werner","family":"Melzer","sequence":"additional","affiliation":[{"name":"Institute of Applied Physiology 1 and 2"},{"name":"Department of Neurology, Ulm University, D-89081 Ulm, Germany 1 and 2"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2014,10,27]]},"reference":[{"key":"2023072623301872200_bib1","doi-asserted-by":"publisher","first-page":"4531","DOI":"10.1073\/pnas.0812661106","article-title":"A retrograde signal from RyR1 alters DHP receptor inactivation and limits window Ca2+ release in muscle fibers of Y522S RyR1 knock-in mice","volume":"106","author":"Andronache","year":"2009","journal-title":"Proc. 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