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Received November 20, 2002
Accepted after revision December 20, 2002
1 Department of Pharmacology and Physiology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, 185 South Orange Avenue, Newark, NJ 07103, USA
2 Department of Pharmacology and Physiology, UMDNJ, New Jersey Medical School, 185 South Orange Avenue, Newark, NJ 07103, USA
* To whom correspondence should be addressed. E-mail: nshiroko{at}umdnj.edu.
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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