{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T13:40:32Z","timestamp":1789911632908,"version":"4.0.1"},"reference-count":45,"publisher":"Rockefeller University Press","issue":"3","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2004,9,1]]},"abstract":"<jats:p>In skeletal muscle, the waveform of Ca2+ release under clamp depolarization exhibits an early peak. Its decay reflects an inactivation, which locally corresponds to the termination of Ca2+ sparks, and is crucial for rapid control. In cardiac muscle, both the frequency of spontaneous sparks (i.e., their activation) and their termination appear to be strongly dependent on the Ca2+ content in the sarcoplasmic reticulum (SR). In skeletal muscle, no such role is established. Seeking a robust measurement of Ca2+ release and a way to reliably modify the SR content, we combined in the same cells the \u201cEGTA\/phenol red\u201d method (Pape et al., 1995) to evaluate Ca2+ release, with the \u201cremoval\u201d method (Melzer et al., 1987) to evaluate release flux. The cytosol of voltage-clamped frog fibers was equilibrated with EGTA (36 mM), antipyrylazo III, and phenol red, and absorbance changes were monitored simultaneously at three wavelengths, affording largely independent evaluations of \u0394[H+] and \u0394[Ca2+] from which the amount of released Ca2+ and the release flux were independently derived. Both methods yielded mutually consistent evaluations of flux. While the removal method gave a better kinetic picture of the release waveform, EGTA\/phenol red provided continuous reproducible measures of calcium in the SR (CaSR). Steady release permeability (P), reached at the end of a 120-ms pulse, increased as CaSR was progressively reduced by a prior conditioning pulse, reaching 2.34-fold at 25% of resting CaSR (four cells). Peak P, reached early during a pulse, increased proportionally much less with SR depletion, decreasing at very low CaSR. The increase in steady P upon depletion was associated with a slowing of the rate of decay of P after the peak (i.e., a slower inactivation of Ca2+ release). These results are consistent with a major inhibitory effect of cytosolic (rather than intra-SR) Ca2+ on the activity of Ca2+ release channels.<\/jats:p>","DOI":"10.1085\/jgp.200409071","type":"journal-article","created":{"date-parts":[[2004,8,30]],"date-time":"2004-08-30T18:57:51Z","timestamp":1093892271000},"page":"239-258","update-policy":"https:\/\/doi.org\/10.1085\/jgp.crossmarkpolicy","source":"Crossref","is-referenced-by-count":36,"title":["How Source Content Determines Intracellular Ca2+ Release Kinetics. Simultaneous Measurement of [Ca2+] Transients and [H+] Displacement in Skeletal Muscle"],"prefix":"10.1085","volume":"124","author":[{"given":"Gonzalo","family":"Pizarro","sequence":"first","affiliation":[{"name":"2Departamento de Biofi\u0301sica, Universidad de la Repu\u0301blica, Facultad de Medicina y Facultad de Ciencias, Montevideo, Uruguay"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eduardo","family":"Ri\u0301os","sequence":"additional","affiliation":[{"name":"1Department of Molecular Biophysics and Physiology, Rush University, Chicago, IL 60612"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2004,8,30]]},"reference":[{"key":"2023072617565415400_BIB1","doi-asserted-by":"crossref","first-page":"151","DOI":"10.1113\/jphysiol.1988.sp017244","volume":"403","year":"1988","journal-title":"J. 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