Delay in granular fusion evoked by repetitive cytosolic Ca2+ spikes in mouse pancreatic acinar cells

Y. Maruyama, O. H. Petersen

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49 Citations (Scopus)


Patch-clamp whole-cell recording in combination with a phase-sensitive detection method was applied to single, enzymatically isolated, mouse pancreatic acinar cells. Either muscarinic stimulation with a low concentration of ACh (50 nM) or cell infusion of inositol 1,4,5-trisphosphate (InsP3) induced repetitive spike-like increases of membrane capacitance (ΔC), membrane conductance (ΔG) and membrane current (ΔI). Cellular perfusion of InsP3, 10 μM in patch-pipettes, induced baseline spikes in ΔC and ΔG, resembling those evoked by ACh. The result indicates that exocytotic granular fusion is primarily triggered by the InsP3-induced repetitive rise of [Ca2+]i. The ACh-induced ΔC took off almost synchronously with ΔG with an apparent delay of less than 40 ms in the initial spike response. This delay of ΔC, however, becomes longer by a factor of 7-12 during repetitive Ca2+ spike cycles. Concomitantly a faster decrease in ΔC spikes than ΔG spikes was observed during the cycles. Two explanations are proposed. First, the Ca2+ sensitivity of granular fusion decreases during the repetitive Ca2+ spikes. This might be due to gradual washout of low molecular components responsible for exocytosis under the whole-cell recording condition. Second, the pool of immediately releasable or of primed zymogen granules is easily exhausted or desensitized during the Ca2+ spike cycles, and has to be supplied from newly primed or sensitized resources. The progressive delay in ΔC during the spike cycle is interpreted as a delay in the process of supplying fusible granules.

Original languageEnglish
Pages (from-to)419-430
Number of pages12
JournalCell Calcium
Issue number5
Publication statusPublished - 1994 Nov

ASJC Scopus subject areas

  • Physiology
  • Molecular Biology
  • Cell Biology


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