• 主题
高级搜索  >
历史搜索 清空历史
首页> 美国卫生研究院文献>British Journal of Pharmacology and Chemotherapy >The mechanism by which monoamine oxidase inhibitors give rise to a non-calcium-dependent component in the depolarization-induced release of 5-HT from rat brain synaptosomes.
【2h】

The mechanism by which monoamine oxidase inhibitors give rise to a non-calcium-dependent component in the depolarization-induced release of 5-HT from rat brain synaptosomes.

机译：单胺氧化酶抑制剂在去极化诱导的大鼠脑突触小体释放5-HT的过程中产生非钙依赖成分的机制。

代理获取
本网站仅为用户提供外文OA文献查询和代理获取服务，本网站没有原文。下单后我们将采用程序或人工为您竭诚获取高质量的原文，但由于OA文献来源多样且变更频繁，仍可能出现获取不到、文献不完整或与标题不符等情况，如果获取不到我们将提供退款服务。请知悉。
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

1. The effects of the monoamine oxidase inhibitors pargyline and nialamide on the Ca2+-dependency of [3H]-5-hydroxytryptamine release from superfused rat brain synaptosomes has been studied in order to evaluate the discrepancies that have occasionally been observed in studying transmitter release by in vivo and in vitro techniques. 2. The application of K+ pulses of low concentration (12.5-20 mM) caused an essentially Ca2+-dependent release of [3H]-5-HT. However, at K+ concentrations above 30 mM, a small non-Ca2+-dependent component appeared. 3. At high concentrations of K+ (30-55 mM), nialamide (18 microM) or pargyline (7 microM) increased the amount of [3H]-5-HT released which could be accounted for by an increase in the non-Ca2+-dependent component of release. 4. The elevation of the non-Ca2+-dependent component of release caused by the monoamine oxidase inhibitors was totally abolished by the inhibitors of the plasma membrane 5-HT carrier, chlomipramine (500 nM), citalopram (50 nM) and fluoxetine (1 microM). 5. The results suggest that the non-Ca2+-dependent component of release seen with high depolarizing concentrations of K+, particularly in the presence of monoamine oxidase inhibitors, is caused by the efflux of [3H]-5-HT through the plasma membrane carrier which seems to be activated during depolarization. 6. The significance of these findings to the physiological in vivo situation, and to the use of in vitro preparations in the study of transmitter release is discussed.
机译：1.研究了单胺氧化酶抑制剂Pargyline和尼拉胺对大鼠超融合突触小体中[3H] -5-羟基色胺释放的Ca2 +依赖性的作用，以评估在研究发射机释放时偶尔观察到的差异。体内和体外技术。 2.低浓度（12.5-20 mM）的K +脉冲的施加导致[3H] -5-HT基本上依赖于Ca2 +的释放。但是，在K +浓度高于30 mM时，会出现小的非Ca2 +依赖性成分。 3.在高浓度的K +（30-55 mM）下，尼酰胺（18 microM）或Pargyline（7 microM）增加了[3H] -5-HT的释放量，这可能是由于非Ca2 +的增加所致依赖于发布的组件。 4.由单胺氧化酶抑制剂引起的非Ca2 +依赖性释放成分的升高已完全被质膜5-HT载体，氯米帕明（500 nM），西酞普兰（50 nM）和氟西汀（1）的抑制剂所消除。 microM）。 5.结果表明，在高去极化浓度的K +下，特别是在存在单胺氧化酶抑制剂的情况下，非Ca2 +依赖性释放成分是由[3H] -5-HT通过质膜载体的流出引起的它似乎在去极化过程中被激活。 6.讨论了这些发现对体内生理状况以及体外制剂在研究递质释放中的意义。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
代理获取

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号