Allgaier C, Schobert A, Belledin M, Jackisch R, Hertting G
Institut für Pharmakologie und Toxikologie, Albert-Ludwigs-Universität Freiburg, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1994 Sep;350(3):258-66. doi: 10.1007/BF00175031.
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)
在本研究中，我们试图全面描述鸡交感神经元去甲肾上腺素释放的调节机制。为此，从鸡腰骶部椎旁神经节分离并培养7天的交感神经元，用0.05 μmol/L的[³H] - 去甲肾上腺素进行加载，然后施加电场刺激（36个脉冲/3 Hz）。由于释放的递质会部分被重摄取，因此通常在去甲肾上腺素再摄取抑制剂（+） - 奥普替林存在的情况下进行灌流。[³H] - 去甲肾上腺素以依赖细胞外Ca²⁺且对河豚毒素（TTX）敏感的方式释放。ω - 芋螺毒素（ω - CTX；100 nmol/L）可消除[³H] - 去甲肾上腺素的释放，表明通过ω - CTX敏感的Ca²⁺通道内流对于递质释放至关重要。1,4 - 二氢 - 2,6 - 二甲基 - 5 - 硝基 - 4 - [2 - （三氟甲基） - 苯基] - 3 - 吡啶羧酸甲酯（（±）Bay K 8644）和4 - （4 - 苯并呋喃基） - 1,4 - 二氢 - 2,6 - 二甲基 - 3 - 硝基 - 5 - 吡啶羧酸异丙酯（（+） - 202 - 791），L型电压敏感Ca²⁺通道（VSCCs）的激动剂，可增加去甲肾上腺素的释放，此外还诱导了一种依赖Ca²⁺且被TTX存在所阻止的氚溢出。L型VSCC拮抗剂（ - ） - 202 - 791和（+） - 4 - （4 - 苯并呋喃基） - 1,4 - 二氢 - 2,6 - 二甲基 - 3,5 - 吡啶二甲酸甲酯、异丙酯（（+） - PN 200 - 110）可减少[³H] - 去甲肾上腺素的释放。这些数据表明，可能位于神经元细胞体上的L型VSCCs在释放调节中起额外作用。（摘要截断于250字）
