尼古丁或钾的长期治疗可减弱人神经母细胞瘤SH-SY5Y细胞去极化诱发的去甲肾上腺素释放。

Chronic treatment with nicotine or potassium attenuates depolarisation-evoked noradrenaline release from the human neuroblastoma SH-SY5Y.

作者信息

Agis-Torres Angel, Ball Stephen G, Vaughan Peter F T

机构信息

Sección Departamental de Fisiología, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain.

出版信息

Neurosci Lett. 2002 Oct 18;331(3):167-70. doi: 10.1016/s0304-3940(02)00881-9.

DOI:10.1016/s0304-3940(02)00881-9

PMID:12383923

Abstract

Chronic treatment, of SH-SY5Y cells, with KCl (20 mM) for 4 days decreased 100 mM KCl-evoked noradrenaline (NA) release by 50% and nicotine (100 microM)-evoked NA release by 55%. Pretreatment with the L-type calcium channel antagonist, nifedipine, prevented this inhibitory effect of chronic exposure to 20 mM KCl on NA release. In contrast pretreatment with 10 microM nicotine for 4 days had no effect on 100 mM KCl -evoked secretion and decreased nicotinic -evoked NA release by only 25%. Inclusion of nifedipine prevented the inhibition of NA release by chronic nicotine treatment. These data are discussed in relation to effects of chronic moderate, depolarisation by either K(+) or nicotine on influx of Ca(2+) via L-type voltage sensitive calcium channels.

摘要

用20 mM KCl对SH-SY5Y细胞进行4天的慢性处理，使100 mM KCl诱发的去甲肾上腺素（NA）释放减少50%，使尼古丁（100 microM）诱发的NA释放减少55%。用L型钙通道拮抗剂硝苯地平预处理可防止长期暴露于20 mM KCl对NA释放的这种抑制作用。相比之下，用10 microM尼古丁预处理4天对100 mM KCl诱发的分泌没有影响，仅使烟碱诱发的NA释放减少25%。加入硝苯地平可防止慢性尼古丁处理对NA释放的抑制。这些数据结合K(+)或尼古丁引起的慢性中度去极化对通过L型电压敏感钙通道的Ca(2+)内流的影响进行了讨论。