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 (iKACh). 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.
|Titolo:||Adenovirus-mediated expression of 5-HT1B receptors in cardiac ventricle myocytes; coupling to inwardly rectifying K+ channels|
|Autori interni:||BARUSCOTTI, MIRKO (Secondo)|
|Parole Chiave:||5-HT(5-hydroxytryptamine, serotonin) ; 5-HT1B receptor ; Muscarinic-gated, inwardly rectifying K+ channel ; Adenylyl cyclase ; Adenovirus ; Ventricle myocyte|
|Settore Scientifico Disciplinare:||Settore BIO/09 - Fisiologia|
|Data di pubblicazione:||1997|
|Digital Object Identifier (DOI):||10.1016/S0014-2999(97)01404-0|
|Appare nelle tipologie:||01 - Articolo su periodico|