Intravesicular calcium transient during calcium release from sarcoplasmic reticulum

• Published in: Biochemistry (Easton) Vol. 30; no. 21; pp. 5230 - 5237
• Main Authors: Ikemoto, Noriaki, Antoniu, Bozena, Kang, Jaw Jou, Meszaros, Laszlo G, Ronjat, Michel
• Format: Journal Article
• Language: English
• Published: Washington, DC American Chemical Society 28.05.1991
• Subjects: Animals; Biological and medical sciences; Caffeine - pharmacology; calcium; Calcium - metabolism; Calsequestrin - metabolism; Cell physiology; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Intracellular Membranes - metabolism; Membrane and intracellular transports; Membrane Proteins - metabolism; Molecular and cellular biology; Murexide - analogs & derivatives; Murexide - metabolism; Polylysine - pharmacology; Rabbits; sarcoplasmic reticulum; Sarcoplasmic Reticulum - metabolism; Intracellular transport; Gel electrophoresis; Rabbit; Ion transport; Lagomorpha; Calcium Ions; Absorption spectrometry; Vertebrata; Stopped flow method; Mammalia; Sarcoplasmic reticulum; Muscle; Kinetics; Release; Cytoplasmic vesicle
• ISSN: 0006-2960; 1520-4995
• DOI: 10.1021/bi00235a017

The time course of changes in the intravesicular Ca2+ concentration ([Ca2+]i) in terminal cisternal sarcoplasmic reticulum vesicles upon the induction of Ca2+ release was investigated by using tetramethylmurexide (TMX) as an intravesicular Ca2+ probe. Upon the addition of polylysine at the concentration that led to the maximum rate of Ca2+ release, [Ca2+]i decreased monotonically in parallel with Ca2+ release. Upon induction of Ca2+ release by lower concentrations of polylysine, [Ca2+]i first increased above the resting level, followed by a decrease well below it. The release triggers polylysine, and caffeine brought about dissociation of calcium that bound to a nonvesicular membrane segment consisting of the junctional face membrane and calsequestrin bound to it, as monitored with TMX. No Ca2+ dissociation from calsequestrin-free junctional face membranes or from the dissociated calsequestrin was produced by release triggers, but upon reassociation of the dissociated calsequestrin and the junctional face membrane, Ca2+ dissociation by triggers was restored. On the basis of these results, we propose that the release triggers elicit a signal in the junctional face membrane, presumably in the foot protein moiety, which is then transmitted to calsequestrin, leading to the dissociation of the bound calcium; and in SR vesicles, to the transient increase of [Ca2+]i, and subsequently release across the membrane.