首页> 外文期刊>American Journal of Physiology >Small conductance Ca2+-activated K+ channels regulate firing properties and excitability in parasympathetic cardiac motoneurons in the nucleus ambiguus.
【24h】

Small conductance Ca2+-activated K+ channels regulate firing properties and excitability in parasympathetic cardiac motoneurons in the nucleus ambiguus.

机译:小电导的Ca2 +激活的K +通道可调节歧义核中副交感神经运动神经元的放电特性和兴奋性。

获取原文
获取原文并翻译 | 示例
           

摘要

Small conductance Ca(2+)-activated K(+) channels (SK) regulate action potential (AP) firing properties and excitability in many central neurons. However, the functional roles of SK channels of parasympathetic cardiac motoneurons (PCMNs) in the nucleus ambiguus have not yet been well characterized. In this study, the tracer X-rhodamine-5 (and 6)-isothiocyanate (XRITC) was injected into the pericardial sac to retrogradely label PCMNs in FVB mice at postnatal days 7-9. Two days later, XRITC-labeled PCMNs in brain stem slices were identified. With the use of whole cell current clamp, single APs and spike trains of different frequencies were evoked by current injections. We found that 1) PCMNs have two different firing patterns: the majority of PCMNs (90%) exhibited spike frequency adaptation (SFA) and the rest (10%) showed less or no adaptation; 2) application of the specific SK channel blocker apamin significantly increased spike half-width in single APs and trains and reduced the spike frequency-dependent AP broadening in trains; 3) SK channel blockade suppressed afterhyperpolarization (AHP) amplitude following single APs and trains and abolished spike-frequency dependence of AHP in trains; and 4) SK channel blockade increased the spike frequency but did not alter the pattern of SFA. Using whole cell voltage clamp, we measured outward currents and afterhyperpolarization current (I(AHP)). SK channel blockade revealed that SK-mediated outward currents had both transient and persistent components. After bath application of apamin and Ca(2+)-free solution, we found that apamin-sensitive and Ca(2+)-sensitive I(AHP) were comparable, confirming that SK channels may contribute to a major portion of Ca(2+)-activated K(+) channel-mediated I(AHP). These results suggest that PCMNs have SK channels that significantly regulate AP repolarization, AHP, and spike frequency but do not affect SFA. We conclude that activation of SK channels underlies one of the mechanisms for negative control of PCMN excitability.
机译:小电导Ca(2+)激活K(+)通道(SK)调节许多中枢神经元的动作电位(AP)放电特性和兴奋性。然而,副交感神经运动神经元(PCMNs)在歧义核中的SK通道的功能作用尚未得到很好的表征。在这项研究中,示踪剂X-rhodamine-5(和6)-异硫氰酸酯(XRITC)被注入心包囊中,以在出生后7-9天逆行标记FVB小鼠中的PCMNs。两天后,在脑干切片中鉴定出XRITC标记的PCMN。通过使用全电池电流钳,通过电流注入可以诱发单个AP和不同频率的峰值串。我们发现1)PCMN具有两种不同的触发模式:大多数PCMN(90%)表现出尖峰频率自适应(SFA),其余(10%)表现出很少或没有自适应; 2)使用特定的SK通道阻断剂apamin显着增加了单个AP和列车中的尖峰半宽度,并减少了列车中与尖峰频率相关的AP展宽; 3)SK信道封锁抑制了单个AP和列车后的超极化(AHP)幅度,并消除了列车中AHP的尖峰频率依赖性; 4)SK通道封锁增加了尖峰频率,但没有改变SFA的模式。使用全电池电压钳,我们测量了向外电流和超极化后电流(I(AHP))。 SK通道封锁显示,SK介导的外向电流既具有瞬态分量又具有持久分量。浴后应用阿帕明和不含Ca(2+)的溶液后,我们发现对阿帕敏和Ca(2+)敏感的I(AHP)具有可比性,证实SK通道可能对Ca(2)的贡献很大+)激活的K(+)通道介导的I(AHP)。这些结果表明PCMN具有SK通道,可显着调节AP复极化,AHP和尖峰频率,但不影响SFA。我们得出结论,SK通道的激活是PCMN兴奋性负控制的机制之一。

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