ADENOVIRUS-MEDIATED EXPRESSION OF 5-HT1B RECEPTORS IN CARDIAC VENTRICLE MYOCYTES - COUPLING TO INWARDLY RECTIFYING K+ CHANNELS

The 5-HT1B receptor is expressed on nerve terminals where it inhibits neurotransmitter release. When expressed ectopically in fibroblasts, t he 5-HT1B receptor inhibits adenylyl cyclase. However, in the central nervous system, the effect of this receptor on neurotransmitter releas e appears to be cAMP-independent. We therefore investigated alternativ e effector systems that might be activated by the 5-HT1B receptor. We constructed a recombinant adenovirus that allows expression of high le vels of the 5-HT1B receptor in a variety of cells. We chose cardiac ve ntricle myocytes because they express a muscarinic-gated, inwardly rec tifying K+ channel (i(KACh)). In infected ventricle cells, both 5-HT a nd the muscarinic receptor agonist, carbachol, elicited a similar inwa rdly rectifying K+ current. The currents elicited by these agonists we re pertussis-toxin sensitive and were not additive. These results sugg est a common signal transduction pathway for 5-HT1B and muscarinic rec eptors in ventricle cells. (C) 1997 Elsevier Science B.V.