期刊
JOURNAL OF PHYSIOLOGY-LONDON
卷 547, 期 2, 页码 453-462出版社
CAMBRIDGE UNIV PRESS
DOI: 10.1113/jphysiol.2002.036129
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资金
- NIAMS NIH HHS [R01 AR045690, R01-AR45690] Funding Source: Medline
In the present study, the link between cellular metabolism and Ca2+ signalling was investigated in permeabilized mammalian skeletal muscle. Spontaneous events of Ca2+ release from the sarcoplasmic reticulum. were detected with fluo-3 and confocal scanning microscopy. Mitochondrial functions were monitored by measuring local changes in mitochondrial membrane potential (with the potential-sensitive dye tetramethylrhodamine ethyl ester) and in mitochondrial [Ca2+] (with the Ca2+ indicator mag-rhod-2). Digital fluorescence imaging microscopy was used to quantify changes in the mitochondrial autofluorescence of NAD(P)H. When fibres were immersed in a solution without mitochondrial substrates, Ca2+ release events were readily observed. The addition of L-glutamate or pyruvate reversibly decreased the frequency of Ca2+ release events and increased mitochondrial membrane potential and NAD(P)H production. Application of various mitochondrial inhibitors led to the loss of mitochondrial [Ca2+] and promoted spontaneous Ca2+ release from the sarcoplasmic reticulum. In many cases, the increase in the frequency of Ca2+ release events was not accompanied by a rise in global [Ca2+](i). Our results suggest that mitochondria exert a negative control over Ca2+ signalling in skeletal muscle by buffering Ca2+ near Ca2+ release channels.
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