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J Biol Chem, Vol. 274, Issue 1, 282-287, January 1, 1999

Modulation of Pancreatic Acinar Cell to Cell Coupling during ACh-evoked Changes in Cytosolic Ca²⁺

Marc Chanson^§, Patrice Mollard^**, Paolo Meda, Susanne Suter^§, and Habo J. Jongsma

From the  Department of Medical Physiology and Sport Medicine, Utrecht University, 3508TA Utrecht, The Netherlands, ^** INSERM Unit 469, CCIPE, 34094 Montpellier, France, and the ^§ Department of Pediatrics and  Department of Morphology, University of Geneva, 1211 Geneva 14, Switzerland

The temporal changes in cytosolic free Ca²⁺ ([Ca²⁺]_i), Ca²⁺-dependent membrane currents (I_m), and gap junctional current (I_j) elicited by acetylcholine (ACh) were measured in rat pancreatic acinar cells using digital imaging and dual perforated patch-clamp recording. ACh (50 nM-5 µM) increased [Ca²⁺]_i and evoked I_m currents without altering I_j in 19 of 37 acinar cell pairs. Although [Ca²⁺]_i rose asynchronously in cells comprising a cluster, the delay of the [Ca²⁺]_i responses decreased with increasing ACh concentrations. Perfusion of inositol 1,4,5-trisphosphate (IP₃) into one cell of a cluster resulted in [Ca²⁺]_i responses in neighboring cells that were not necessarily in direct contact with the stimulated one. This suggests that extensive coupling between acinar cells provides a pathway for cell-to-cell diffusion of Ca²⁺-releasing signals. Strikingly, maximal (1-5 µM) ACh concentrations reduced I_j by 69 ± 15% (n = 9) in 25% of the cell pairs subjected to dual patch-clamping. This decrease occurred shortly after the I_m peak and was prevented by incubating acinar cells in a Ca²⁺-free medium, suggesting that uncoupling was subsequent to the initiation of the Ca²⁺-mobilizing responses. Depletion of Ca²⁺-sequestering stores by thapsigargin resulted in a reduction of intercellular communication similar to that observed with ACh. In addition, ACh-induced uncoupling was prevented by blocking nitric oxide production with L-nitro-arginine and restored by exposing acinar cells to dibutyryl cGMP. The results suggest that ACh-induced uncoupling and capacitative Ca²⁺ entry are regulated concurrently. Closure of gap junction channels may occur to functionally isolate nearby cells differing in their intrinsic sensitivity to ACh and thereby to allow for sustained activity of groups of secreting cells.

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