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ludc web

Lena Eliasson

Principal investigator

ludc web

CaM kinase II-dependent mobilization of secretory granules underlies acetylcholine-induced stimulation of exocytosis in mouse pancreatic B-cells

Author

  • Jesper Gromada
  • Marianne Hoy
  • Erik Renström
  • Krister Bokvist
  • Lena Eliasson
  • Sven Göpel
  • Patrik Rorsman

Summary, in English

1. Measurements of cell capacitance were used to investigate the mechanisms by which acetylcholine (ACh) stimulates Ca2+-induced exocytosis in single insulin-secreting mouse pancreatic B-cells. 2. ACh (250 microM) increased exocytotic responses elicited by voltage-clamp depolarizations 2.3-fold. This effect was mediated by activation of muscarinic receptors and dependent on elevation of the cytoplasmic Ca2+ concentration ([Ca2+]i) attributable to mobilization of Ca2+ from intracellular stores. The latter action involved interference with the buffering of [Ca2+]i and the time constant (tau) for the recovery of [Ca2+]i following a voltage-clamp depolarization increased 5-fold. As a result, Ca2+ was present at concentrations sufficient to promote the replenishment of the readily releasable pool of granules (RRP; > 0.2 microM) for much longer periods in the presence than in the absence of the agonist. 3. The effect of Ca2+ on exocytosis was mediated by activation of CaM kinase II, but not protein kinase C, and involved both an increased size of the RRP from 40 to 140 granules and a decrease in tau for the refilling of the RRP from 31 to 19 s. 4. Collectively, the effects of ACh on the RRP and tau result in a > 10-fold stimulation of the rate at which granules are supplied for release.

Department/s

  • Diabetes - Islet Patophysiology
  • Diabetes - Islet Cell Exocytosis
  • Department of Experimental Medical Science
  • Islet cell physiology

Publishing year

1999

Language

English

Pages

745-759

Publication/Series

Journal of Physiology

Volume

518

Issue

3

Document type

Journal article

Publisher

The Physiological Society

Topic

  • Physiology

Status

Published

Research group

  • Diabetes - Islet Patophysiology
  • Diabetes - Islet Cell Exocytosis
  • Islet cell physiology

ISBN/ISSN/Other

  • ISSN: 1469-7793