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Title: Phenolamine-dependent adenylyl cyclase activation in Drosophila Schneider 2 cells
Authors: Van Poyer, Wendy ×
Torfs, Herbert
Poels, Jeroen
Swinnen, Elfriede
De Loof, Arnold
Akerman, K
Vanden Broeck, Jozef #
Issue Date: Mar-2001
Series Title: Insect biochemistry and molecular biology. vol:31 issue:4-5 pages:333-8
Abstract: Drosophila Schneider 2 (S2) cells are often employed as host cells for non-lytic, stable expression and functional characterization of mammalian and insect G-protein-coupled receptors (GPCRs), such as biogenic amine receptors. In order to avoid cross-reactions, it is extremely important to know which endogenous receptors are already present in the non-transfected S2 cells. Therefore, we analyzed cellular levels of cyclic AMP and Ca2+, important second messengers for intracellular signal transduction via GPCRs, in response to a variety of naturally occurring biogenic amines, such as octopamine, tyramine, serotonin, histamine, dopamine and melatonin. None of these amines (up to 0.1 mM) was able to reduce forskolin-stimulated cyclic AMP production in S2 cells. Furthermore, no agonist-induced calcium responses were observed. Nevertheless, the phenolamines octopamine (OA) and tyramine (TA) induced a dose-dependent increase of cyclic adenosine monophosphate (AMP) production in S2 cells, while serotonin, histamine, dopamine and melatonin (up to 0.1 mM) did not. The pharmacology of this response was similar to that of the octopamine-2 (OA2) receptor type. In addition, this paper provides evidence for the presence of an endogenous mRNA encoding an octopamine receptor type in these cells, which is identical or very similar to OAMB. This receptor was previously shown to be positively coupled to adenylyl cyclase.
URI: 
ISSN: 0965-1748
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Animal Physiology and Neurobiology Section - miscellaneous
Department of Biology - miscellaneous
Pharmacology Section (-)
Laboratory for Molecular Diagnosis
× corresponding author
# (joint) last author

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