cAMP potentiates InsP3-induced Ca2+release from the endoplasmic reticulum in blowfly salivary glands
✍ Scribed by Ruth Schmidt; Otto Baumann; Bernd Walz
- Publisher
- BioMed Central
- Year
- 2008
- Tongue
- English
- Weight
- 352 KB
- Volume
- 8
- Category
- Article
- ISSN
- 1472-6793
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Background
Serotonin induces fluid secretion from Calliphora salivary glands by the parallel activation of the InsP~3~/Ca^2+^ and cAMP signaling pathways. We investigated whether cAMP affects 5-HT-induced Ca^2+^ signaling and InsP~3~-induced Ca^2+^ 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 [Ca^2+^]~i~ changes into a sustained increase. Intraluminal Ca^2+^ measurements in the ER of β-escin-permeabilized glands with mag-fura-2 revealed that cAMP augmented InsP~3~-induced Ca^2+^ release in a concentration-dependent manner. This indicated that cAMP sensitized the InsP~3~ receptor Ca^2+^ channel for InsP~3~. 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 InsP~3~-induced Ca^2+^ release was mediated by PKA not by Epac. Recordings of the transepithelial potential of the glands suggested that cAMP sensitized the InsP~3~/Ca^2+^ signaling pathway for 5-HT, because IBMX potentiated Ca^2+^-dependent Cl^-^ transport activated by a threshold 5-HT concentration.
Conclusion
This report shows, for the first time for an insect system, that cAMP can potentiate InsP~3~-induced Ca^2+^ release from the ER in a PKA-dependent manner, and that this crosstalk between cAMP and InsP~3~/Ca^2+^ signaling pathways enhances transepithelial electrolyte transport.