Pertussis toxin abolishes the inhibition of Ca2+ currents and of noradrenaline release via α2-adrenoceptors in chick sympathetic neurons

SummaryEffects of α2-adrenoceptor agonists on whole-cell Ca2+ currents and 3H-noradrenaline release were investigated by applying the patch-clamp technique and electrical field stimulation to cultured embryonic chick sympathetic neurons. A 24-h exposure of the sympathetic neurons to pertussis toxin (100 ng/ml) abolished both the α2-adrenoceptor-mediated inhibition of Ca 2+ currents and the modulation of noradrenaline release caused by noradrenaline (1 μmol/l; in the presence of 10 μmol/l cocaine) or the α2-adrenoceptor agonists 5-bromo-6-(2imidazolin-2-ylamino)quinoxaline (UK 14,304, 10 μmol/ l) and clonidine (10 μmol/l). These results suggest that the α2-autoreceptor-mediated inhibition of noradrenaline release from chick sympathetic neurons operates through the modulation of Ca2+ channels via pertussistoxin-sensitive GTP-binding-proteins.