title: In vivo Ca2+dynamics induced by Ca2+injection in individual rat skeletal muscle fibers.
abstract: In contrast to cardiomyocytes, store overload-induced calcium ion (Ca2+) release (SOICR) is not considered to constitute a primary Ca2+releasing system from the sarcoplasmic reticulum (SR) in skeletal muscle myocytes. In the latter, voltage-induced Ca2+release (VICR) is regarded as the dominant mechanism facilitating contractions. Any role of the SOICR in the regulation of cytoplasmic Ca2+concentration ([Ca2+]i) and its dynamics in skeletal muscle in vivo remains poorly understood. By means of in vivo single fiber Ca2+microinjections combined with bioimaging techniques, we tested the hypothesis that the [Ca2+]idynamics following Ca2+injection would be amplified and fiber contraction facilitated by SOICR. The circulation-intact spinotrapezius muscle of adult male Wistar rats (n=34) was exteriorized and loaded with Fura-2 AM to monitor [Ca2+]idynamics. Groups of rats underwent the following treatments: (1) 0.02, 0.2, and 2.0 mmol/L Ca2+injections, (2) 2.0 mmol/L Ca2+with inhibition of ryanodine receptors (RyR) by dantrolene sodium (DAN), and (3) 2.0 mmol/L Ca2+with inhibition of SR Ca2+ATPase (SERCA) by cyclopiazonic acid (CPA). A quantity of 0.02 mmol/L Ca2+injection yielded no detectable response, whereas peak evoked [Ca2+]iincreased 9.9 ± 1.8% above baseline for 0.2 mmol/L and 23.8 ± 4.3% (P< 0.05) for 2.0 mmol/L Ca2+injections. The peak [Ca2+]iin response to 2.0 mmol/L Ca2+injection was largely abolished by DAN and CPA (-85.8%, -71.0%, respectively, bothP< 0.05 vs. unblocked) supporting dependence of the [Ca2+]idynamics on Ca2+released by SOICR rather than injected Ca2+itself. Thus, this investigation demonstrates the presence of a robust SR-evoked SOICR operant in skeletal muscle in vivo.
authors.affiliation: Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Chofu, Tokyo, Japan.
authors.forename: Mario
authors.initials: M
authors.lastname: Wakizaka
authors.affiliation: Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Chofu, Tokyo, Japan.|Department of Metabolism and Endocrinology, Juntendo University Graduate School of Medicine, Hongo, Tokyo, Japan.
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Eshima
authors.affiliation: Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Chofu, Tokyo, Japan.
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Tanaka
authors.affiliation: Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Chofu, Tokyo, Japan.
authors.forename: Hideki
authors.initials: H
authors.lastname: Shirakawa
authors.affiliation: Departments of Anatomy & Physiology and Kinesiology, Kansas State University, Manhattan, Kansas.
authors.forename: David C
authors.initials: DC
authors.lastname: Poole
authors.affiliation: Department of Engineering Science, Bioscience and Technology Program, University of Electro-Communications, Chofu, Tokyo, Japan kano@pc.uec.ac.jp.
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kano
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000187:drug effects / Q000378:metabolism*; D009287:Naphthyridines / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases / Q000037:antagonists & inhibitors
chemical_list: C516002:2,7-diamido-1,8-naphthyridine; D002121:Calcium Channel Blockers; D009287:Naphthyridines; D019837:Ryanodine Receptor Calcium Release Channel; D053498:Sarcoplasmic Reticulum Calcium-Transporting ATPases; D002118:Calcium
keywords: Ca2+‐induced Ca2+ release; ryanodine receptor; sarcoplasmic reticulum; store overload‐induced Ca2+ release