Abstract
Using dual excitation and fixed emission fluorescence microscopy, we were able to measure changes in cytoplasmic free Ca2+ concentration ([Ca2+]i) and mitochondrial membrane potential simultaneously in the pancreatic β-cell. The β-cells were exposed to a combination of the Ca2+ indicator fura-2/AM and the indicator of mitochondrial membrane potential, rhodamine 123 (Rh123). Using simultaneous measurements of mitochondrial membrane potential and [Ca2+] i during glucose stimulation, it was possible to measure the time lag between the onset of mitochondrial hyperpolarization and changes in [Ca 2+]i. Glucose-induced oscillations in [Ca 2+]i were followed by transient depolarizations of mitochondrial membrane potential. These results are compatible with a model in which nadirs in [Ca2+]i oscillations are generated by a transient, Ca2+-induced inhibition of mitochondrial metabolism resulting in a temporary fall in the cytoplasmic ATP/ADP ratio, opening of plasma membrane KATP channels, repolarization of the plasma membrane, and thus transient closure of voltage-gated L-type Ca2+ channels.
| Original language | English |
|---|---|
| Pages (from-to) | 34530-34536 |
| Number of pages | 7 |
| Journal | Journal of Biological Chemistry |
| Volume | 276 |
| Issue number | 37 |
| DOIs | |
| State | Published - Sep 14 2001 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Biochemistry
Cite this
Glucose-induced Oscillations in Cytoplasmic Free Ca2+ Concentration Precede Oscillations in Mitochondrial Membrane Potential in the Pancreatic β-Cell. / Kindmark, Henrik; Köhler, Martin; Brown, Graham; Bränström, Robert; Larsson, Olof; Berggren, Per Olof.
In: Journal of Biological Chemistry, Vol. 276, No. 37, 14.09.2001, p. 34530-34536.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Glucose-induced Oscillations in Cytoplasmic Free Ca2+ Concentration Precede Oscillations in Mitochondrial Membrane Potential in the Pancreatic β-Cell
AU - Kindmark, Henrik
AU - Köhler, Martin
AU - Brown, Graham
AU - Bränström, Robert
AU - Larsson, Olof
AU - Berggren, Per Olof
PY - 2001/9/14
Y1 - 2001/9/14
N2 - Using dual excitation and fixed emission fluorescence microscopy, we were able to measure changes in cytoplasmic free Ca2+ concentration ([Ca2+]i) and mitochondrial membrane potential simultaneously in the pancreatic β-cell. The β-cells were exposed to a combination of the Ca2+ indicator fura-2/AM and the indicator of mitochondrial membrane potential, rhodamine 123 (Rh123). Using simultaneous measurements of mitochondrial membrane potential and [Ca2+] i during glucose stimulation, it was possible to measure the time lag between the onset of mitochondrial hyperpolarization and changes in [Ca 2+]i. Glucose-induced oscillations in [Ca 2+]i were followed by transient depolarizations of mitochondrial membrane potential. These results are compatible with a model in which nadirs in [Ca2+]i oscillations are generated by a transient, Ca2+-induced inhibition of mitochondrial metabolism resulting in a temporary fall in the cytoplasmic ATP/ADP ratio, opening of plasma membrane KATP channels, repolarization of the plasma membrane, and thus transient closure of voltage-gated L-type Ca2+ channels.
AB - Using dual excitation and fixed emission fluorescence microscopy, we were able to measure changes in cytoplasmic free Ca2+ concentration ([Ca2+]i) and mitochondrial membrane potential simultaneously in the pancreatic β-cell. The β-cells were exposed to a combination of the Ca2+ indicator fura-2/AM and the indicator of mitochondrial membrane potential, rhodamine 123 (Rh123). Using simultaneous measurements of mitochondrial membrane potential and [Ca2+] i during glucose stimulation, it was possible to measure the time lag between the onset of mitochondrial hyperpolarization and changes in [Ca 2+]i. Glucose-induced oscillations in [Ca 2+]i were followed by transient depolarizations of mitochondrial membrane potential. These results are compatible with a model in which nadirs in [Ca2+]i oscillations are generated by a transient, Ca2+-induced inhibition of mitochondrial metabolism resulting in a temporary fall in the cytoplasmic ATP/ADP ratio, opening of plasma membrane KATP channels, repolarization of the plasma membrane, and thus transient closure of voltage-gated L-type Ca2+ channels.
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UR - http://www.scopus.com/inward/citedby.url?scp=0035860699&partnerID=8YFLogxK
U2 - 10.1074/jbc.M102492200
DO - 10.1074/jbc.M102492200
M3 - Article
VL - 276
SP - 34530
EP - 34536
JO - Journal of Biological Chemistry
JF - Journal of Biological Chemistry
SN - 0021-9258
IS - 37
ER -