...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>The European Journal of Neuroscience >The time course of transmitter release in mouse motor nerve terminals is differentially affected by activation of muscarinic M1 or M2 receptors.
【24h】

The time course of transmitter release in mouse motor nerve terminals is differentially affected by activation of muscarinic M1 or M2 receptors.

机译：毒蕈碱M1或M2受体的激活会不同程度地影响小鼠运动神经末梢释放递质的时间。

获取原文
获取原文并翻译 | 示例
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

At endplates of mouse diaphragms the effects of activation of presynaptic muscarinic M1 and M2 autoreceptors on the time courses of monoquantal releases have been investigated at 20 degrees C. Quantal excitatory postsynaptic currents (qEPSCs) were elicited and recorded with a perfused macropatch electrode, through which control- and drug-containing solutions were applied to 10 microm phi regions of a neuromuscular junction. M2 receptors were activated with muscarine, while the M1 receptors were blocked by pirenzepine. M2 activation presented a slight, but highly significant augmentation of early releases. Analogously, M1 receptors were activated with muscarine, while M2 receptors were blocked by methoctramine. M1 activation elicited a highly significant small shift of the time course of release towards longer delays. In controls, the number of late releases decayed with a time constant of 0.3 ms. This time constant did not change appreciably when methoctramine or methoctramine + muscarine were applied.However, methoctramine + muscarine reduced the amplitude of qEPSCs and shortened their decay by a partial block of postsynaptic channels. Double blocks with pirenzepine + methoctramine allowed no presynaptic effect of muscarine, showing that the blocker concentrations were sufficient. Neither the addition of methoctramine to pirenzepine, nor the further addition of muscarine changed the time constant of decay of the number of late releases. The results are very similar to that of autoreceptor activations in the glutamatergic crayfish synapse: activation of inhibitory receptors augmented early releases, and that of facilitatory receptors depressed early releases [J. Dudel (2006a) Eur. J. Neurosci., 23, 2695-2700], which may suggest a general presynaptic mechanism.
机译：在小鼠diaphragm肌的终板，在20摄氏度下研究了突触前毒蕈碱M1和M2自身受体的激活对单量子释放时间进程的影响。通过灌注的大斑片电极引发并记录了量子兴奋性突触后电流（qEPSC），将含对照和含药物的溶液应用于神经肌肉接头的10 microm phi区域。 M2受体被毒蕈碱激活，而M1受体被哌仑西平阻断。 M2激活显示了早期版本的轻微但非常重要的增强。类似地，M1受体被毒蕈碱激活，而M2受体被甲辛胺阻断。 M1激活引起释放时间进程朝着更长的延迟高度显着的小变化。在对照中，延迟释放的数量以0.3 ms的时间常数衰减。当使用甲基辛特拉明或甲基辛特拉明+毒蕈碱时，该时间常数没有明显变化，但是，甲基辛特拉明+毒蕈碱可降低qEPSC的幅度并通过突触后通道的部分阻滞缩短其衰减。用哌仑西平+甲基辛特拉明双重阻滞剂无毒蕈碱的突触前作用，表明阻滞剂浓度足够。向哌仑西平中添加甲基辛巴明，或进一步添加毒蕈碱都不会改变延迟释放数量衰减的时间常数。结果与谷氨酸能小龙虾突触中的自体受体激活非常相似：抑制性受体的激活增加了早期释放，而促进性受体的激活则抑制了早期释放[J. Chem.Sci。，2002，2，1，3，6。 Dudel（2006a）欧洲。 J. Neurosci。，23，2695-2700]，这可能暗示了一般的突触前机制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

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