Pertussis toxin abolishes the inhibition of Ca2+ currents and of noradrenaline release via alpha 2-adrenoceptors in chick sympathetic neurons.
Effects of alpha 2-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 alpha 2-adrenoceptor-mediated inhibition of Ca2+ currents and the modulation of noradrenaline release caused by noradrenaline (1 mumol/l; in the presence of 10 mumol/l cocaine) or the alpha 2-adrenoceptor agonists 5-bromo-6-(2-imidazolin-2- ylamino)quinoxaline (UK 14,304, 10 mumol/l) and clonidine (10 mumol/l). These results suggest that the alpha 2-autoreceptor-mediated inhibition of noradrenaline release from chick sympathetic neurons operates through the modulation of Ca2+ channels via pertussis-toxin-sensitive GTP-binding-proteins.
Institute of Neuropharmacology, University of Vienna, Austria.
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Boehm
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Huck
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Drobny
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Singer
D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002478:Cells, Cultured; D002642:Chick Embryo; D009638:Norepinephrine / Q000378:metabolism*; D037342:Pertussis Toxin; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000378:metabolism; D014316:Tritium; D010566:Virulence Factors, Bordetella / Q000633:toxicity*
D000316:Adrenergic alpha-Agonists; D011942:Receptors, Adrenergic, alpha; D010566:Virulence Factors, Bordetella; D014316:Tritium; D037342:Pertussis Toxin; D002118:Calcium; D009638:Norepinephrine