title: Modulation of electrically evoked [3H]-noradrenaline release from cultured chick sympathetic neurons.
abstract: In the present study we attempted a comprehensive characterization of modulation of noradrenaline release from chick sympathetic neurons. To this purpose sympathetic neurons derived from chick lumbosacral paravertebral ganglia and kept in culture for 7 days were loaded with 0.05 mumol/l [3H]-noradrenaline and subjected to electrical field stimulation (36 pulses/3 Hz). Since the released transmitter was partially recaptured, superfusion was usually performed in the presence of (+)-oxaprotiline, an inhibitor of noradrenaline re-uptake. [3H]-Noradrenaline was released in a manner which was dependent on extracellular Ca2+ and sensitive to tetrodotoxin (TTX). omega-Conotoxin (omega-CTX; 100 nmol/l) abolished [3H]-noradrenaline release indicating that influx through omega-CTX-sensitive Ca(2+)-channels was essential for transmitter release. 1,4-dihydro-2,6-dimethyl-5-nitro-4-[2- (trifluoromethyl)-phenyl]-3-pyridine carboxylic acid methyl ester ((+/-) Bay K 8644) and 4-(4-benzofurazanyl)-1,4-dihydro-2,6- dimethyl-3-nitro-5-pyridinecarboxylic acid isopropyl ester ((+)-202-791), agonists at L-type voltage sensitive Ca(2+)-channels (VSCCs), increased noradrenaline release and induced, in addition, an overflow of tritium which was Ca(2+)-dependent and prevented by the presence of TTX. The L-type VSCC antagonists (-)-202-791 and (+)-4-(4-benzofurazanyl)-1,4-dihydro-2,6-dimethyl-3,5- pyridinedicar boxylic acid methyl, isopropyl ester) ((+)-PN 200-110) diminished [3H]-noradrenaline release. These data suggest that L-type VSCCs, probably located on the cell body of the neuron, play an additional role in modulation of release.(ABSTRACT TRUNCATED AT 250 WORDS)
authors: Institut für Pharmakologie und Toxikologie, Albert-Ludwigs-Universität Freiburg, Germany.
authors: C
authors: C
authors: Allgaier
authors: A
authors: A
authors: Schobert
authors: M
authors: M
authors: Belledin
authors: R
authors: R
authors: Jackisch
authors: G
authors: G
authors: Hertting
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000818:Animals; D000068438:Brimonidine Tartrate; D002118:Calcium / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism / Q000502:physiology; D002478:Cells, Cultured; D002642:Chick Embryo; D003000:Clonidine / Q000494:pharmacology; D004558:Electric Stimulation; D007545:Isoproterenol / Q000494:pharmacology; D009474:Neurons / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism*; D011810:Quinoxalines / Q000494:pharmacology; D011941:Receptors, Adrenergic / Q000187:drug effects / Q000502:physiology; D017470:Receptors, Glutamate / Q000502:physiology; D012680:Sensitivity and Specificity; D013564:Sympathetic Nervous System / Q000166:cytology / Q000378:metabolism*; D013696:Temperature; D013779:Tetrodotoxin / Q000494:pharmacology; D014316:Tritium
chemical_list: D000316:Adrenergic alpha-Agonists; D015220:Calcium Channels; D011810:Quinoxalines; D011941:Receptors, Adrenergic; D017470:Receptors, Glutamate; D014316:Tritium; D013779:Tetrodotoxin; D000068438:Brimonidine Tartrate; D007545:Isoproterenol; D003000:Clonidine; D002118:Calcium; D009638:Norepinephrine