Abstract
Cholecystokinin (CCK) is one of several active peptides that have been isolated from both the gut1 and the brain2. CCK evokes membrane depolarization and conductance increase in both pancreatic acinar cells3,4 and pyramidal neurones of hippocampus5. In the acinar cells, activation of cholinergic muscarinic and two different peptidergic receptor sites (for CCK and bombesin) result in the same type of conductance increase6. The application of intracellular Ca mimics the action of the agonists7 and Ca has been proposed as an intracellular mediator for the membrane conductance increase8. A cation channel activated by internal Ca has been directly demonstrated in single-channel current recording experiments on isolated patches of plasma membrane from the basolateral surface of pancreatic acini9. We now demonstrate that CCK and acetylcholine (ACh) can activate these inward current channels indirectly. Single-channel currents were observed in electrically isolated membrane patches in situ when micropipette application of CCK or ACh was made outside the patch area. Single-channel currents from the same membrane patches were subsequently recorded after they had been excised (inside-out) and identical values for the single-channel conductance were obtained (∼35 pS). No effect of CCK was obtained in the presence of the specific receptor antagonist dibutyryl cyclic GMP10–12 although in all such cases single-channel currents were subsequently recorded from the excised patch (Ca-activated). These results demonstrate directly that CCK and ACh control ion channel opening via an intracellular messenger (Ca).
This is a preview of subscription content, access via your institution
Access options
Subscribe to this journal
Receive 51 print issues and online access
$199.00 per year
only $3.90 per issue
Buy this article
- Purchase on Springer Link
- Instant access to full article PDF
Prices may be subject to local taxes which are calculated during checkout
Similar content being viewed by others
References
Mutt, V. & Jorpes, J. E. Eur. J. Biochem. 6, 156–162 (1968).
Dockray, G. J., Gregory, R. A., Hutchison, J. B., Harris, J. I. & Runswick, M. J. Nature 274, 711–713 (1978).
Petersen, O. H. Nature new Biol. 244, 73 (1973).
Nishiyama, A. & Petersen, O. H. J. Physiol., Lond. 238, 145–158 (1974).
Dodd, J. & Kelly, J. S. Brain Res. 205, 337–350 (1981).
Petersen, O. H. & Philpott, H. G. J. Physiol., Lond. 290, 305–315 (1979).
Iwatsuki, N. & Petersen, O. H. Nature 268, 147–149 (1977).
Petersen, O. H. & Iwatsuki, N. Ann. N. Y. Acad. Sci. 307, 599–617 (1978).
Maruyama, Y. & Petersen, O. H. Nature 299, 159–161 (1982).
Peikin, S. R., Costenbader, C. L. & Gardner, J. D. J. biol. Chem. 254, 5321–5327 (1979).
Philpott, H. G. & Petersen, O. H. Pflügers Arch. ges. Physiol. 382, 263–267 (1979).
Jensen, R. T., Lemp, G. F. & Gardner, J. D. Proc. natn. Acad. Sci. U.S.A. 77, 2079–2083 (1980).
Williams, J. A., Korc, M. & Dormer, R. L. Am. J. Physiol. 235, E517–524 (1978).
Wakasugi, H. et al. J. Membrane Biol. 65, 205–220 (1982).
Neher, E. in Techniques in Cellular Physiology (ed. Baker, P. F.) Vol. 1, Pt. II, 121, 1–16 (Elsevier, Amsterdam, 1982).
Hamill, O. P., Marty, A., Neher, E., Sakmann, B. & Sigworth, F. J. Pflügers Arch. ges. Physiol. 391, 85–100 (1981).
Petersen, O. H. The Electrophysiology of Gland Cells (Academic, London, 1980).
Bolender, R. P. J. Cell Biol. 61, 269–287 (1974).
Colquhoun, D., Neher, E., Reuter, H. & Stevens, C. F. Nature 294, 752–754 (1981).
Yellen, G. Nature 296, 357–359 (1982).
Petersen, O. H. et al. Phil. Trans. R. Soc. B296, 151–166 (1981).
Li, J. H.-Y., Palmer, L. G., Edelman, I. S. & Lindemann, B. J. Membrane Biol. 64, 77–89 (1982).
Palmer, L. G., Li, J. H.-Y., Lindemann, B. & Edelman, I. S. J. Membrane Biol. 64, 91–102 (1982).
Philpott, H. G. & Petersen, O. H. Nature 281, 684–686 (1979).
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Maruyama, Y., Petersen, O. Cholecystokinin activation of single-channel currents is mediated by internal messenger in pancreatic acinar cells. Nature 300, 61–63 (1982). https://doi.org/10.1038/300061a0
Received:
Accepted:
Issue Date:
DOI: https://doi.org/10.1038/300061a0
This article is cited by
-
Depletion of 14-3-3γ reduces the surface expression of Transient Receptor Potential Melastatin 4b (TRPM4b) Channels and attenuates TRPM4b-mediated glutamate-induced neuronal cell death
Molecular Brain (2014)
-
Specific mitochondrial functions in separate sub-cellular domains of pancreatic acinar cells
Pflügers Archiv - European Journal of Physiology (2012)
-
From Galvani to patch clamp: the development of electrophysiology
Pflügers Archiv - European Journal of Physiology (2006)
-
On the activation mechanism of store-operated calcium channels
Pflügers Archiv - European Journal of Physiology (2006)
-
Ca2+ signalling and membrane current activated by cADPr in starfish oocytes
Pflügers Archiv - European Journal of Physiology (2003)
Comments
By submitting a comment you agree to abide by our Terms and Community Guidelines. If you find something abusive or that does not comply with our terms or guidelines please flag it as inappropriate.
