Articles > cAMP potentiates InsP3-induced Ca2+ release from the endoplasmic reticulum in blowfly salivary glands

cAMP potentiates InsP3-induced Ca2+ release from the endoplasmic reticulum in blowfly salivary glands

cAMP potentiates InsP3-induced Ca2+ release from the endoplasmic reticulum in blowfly salivary glands

Ruth Schmidt, Otto Baumann and Bernd Walz

Institute
of Biochemistry and Biology, Department of Animal Physiology,
University of Potsdam, Karl-Liebknecht-Str. 24-25, 14476 Potsdam-Golm,
Germany

BMC Physiology 2008,
8:10. This is an Open Access article distributed under the terms of the Creative Commons Attribution License.

 

Abstract

Background

Serotonin induces fluid secretion from Calliphora salivary glands by the parallel activation of the InsP3/Ca2+ and cAMP signaling pathways. We investigated whether cAMP affects 5-HT-induced Ca2+ signaling and InsP3-induced Ca2+ release from the endoplasmic reticulum (ER).

Results

Increasing intracellular cAMP level by bath application of
forskolin, IBMX or cAMP in the continuous presence of threshold 5-HT
concentrations converted oscillatory [Ca2+]i changes into a sustained increase. Intraluminal Ca2+ measurements in the ER of β-escin-permeabilized glands with mag-fura-2 revealed that cAMP augmented InsP3-induced Ca2+ release in a concentration-dependent manner. This indicated that cAMP sensitized the InsP3 receptor Ca2+ channel for InsP3.
By using cAMP analogs that activated either protein kinase A (PKA) or
Epac and the application of PKA-inhibitors, we found that cAMP-induced
augmentation of InsP3-induced Ca2+ release was
mediated by PKA not by Epac. Recordings of the transepithelial
potential of the glands suggested that cAMP sensitized the InsP3/Ca2+ signaling pathway for 5-HT, because IBMX potentiated Ca2+-dependent Cltransport activated by a threshold 5-HT concentration.

Conclusion

This report shows, for the first time for an insect system, that cAMP can potentiate InsP3-induced Ca2+ release from the ER in a PKA-dependent manner, and that this crosstalk between cAMP and InsP3/Ca2+ signaling pathways enhances transepithelial electrolyte transport.

 


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