Adenovirus-mediated expression of 5-HT1B receptors in cardiac ventricle myocytes; coupling to inwardly rectifying K+ channels

European Journal of Pharmacology
A GhavamiR Hen

Abstract

The 5-HT1B receptor is expressed on nerve terminals where it inhibits neurotransmitter release. When expressed ectopically in fibroblasts, the 5-HT1B receptor inhibits adenylyl cyclase. However, in the central nervous system, the effect of this receptor on neurotransmitter release appears to be cAMP-independent. We therefore investigated alternative effector systems that might be activated by the 5-HT1B receptor. We constructed a recombinant adenovirus that allows expression of high levels of the 5-HT1B receptor in a variety of cells. We chose cardiac ventricle myocytes because they express a muscarinic-gated, inwardly rectifying K+ channel (i[KACh]). In infected ventricle cells, both 5-HT and the muscarinic receptor agonist, carbachol, elicited a similar inwardly rectifying K+ current. The currents elicited by these agonists were pertussis-toxin sensitive and were not additive. These results suggest a common signal transduction pathway for 5-HT1B and muscarinic receptors in ventricle cells.

References

Apr 1, 1992·Proceedings of the National Academy of Sciences of the United States of America·L MaroteauxR Hen
Jul 1, 1991·Proceedings of the National Academy of Sciences of the United States of America·A KarschinH A Lester
Sep 1, 1987·Naunyn-Schmiedeberg's Archives of Pharmacology·G J MolderingsM Göthert
Jun 1, 1995·Naunyn-Schmiedeberg's Archives of Pharmacology·H ItoM Endoh
Dec 1, 1994·Neurochemistry International·F Saudou, R Hen

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Citations

Dec 26, 2001·Brain Research Bulletin·K A Berg, W P Clarke
Apr 5, 2019·ACS Chemical Neuroscience·Yusha LiuJohn F Neumaier

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