
Anna Edlund
Affiliated researcher

Calcium Current Inactivation Rather than Pool Depletion Explains Reduced Exocytotic Rate with Prolonged Stimulation in Insulin-Secreting INS-1 832/13 Cells.
Author
Summary, in English
Impairment in beta-cell exocytosis is associated with reduced insulin secretion and diabetes. Here we aimed to investigate the dynamics of Ca2+-dependent insulin exocytosis with respect to pool depletion and Ca2+-current inactivation. We studied exocytosis, measured as increase in membrane capacitance (ΔCm), as a function of calcium entry (Q) in insulin secreting INS-1 832/13 cells using patch clamp and mixed-effects statistical analysis. The observed linear relationship between ΔCm and Q suggests that Ca2+-channel inactivation rather than granule pool restrictions is responsible for the decline in exocytosis observed at longer depolarizations. INS-1 832/13 cells possess an immediately releasable pool (IRP) of ∼10 granules and most exocytosis of granules occurs from a large pool. The latter is attenuated by the calcium-buffer EGTA, while IRP is unaffected. These findings suggest that most insulin release occurs away from Ca2+-channels, and that pool depletion plays a minor role in the decline of exocytosis upon prolonged stimulation.
Department/s
- Diabetes - Islet Cell Exocytosis
- EXODIAB: Excellence of Diabetes Research in Sweden
Publishing year
2014
Language
English
Publication/Series
PLoS ONE
Volume
9
Issue
8
Full text
Links
Document type
Journal article
Publisher
Public Library of Science
Topic
- Endocrinology and Diabetes
Status
Published
Research group
- Diabetes - Islet Cell Exocytosis
ISBN/ISSN/Other
- ISSN: 1932-6203