...
  • 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 >Brain-derived neurotrophic factor induces long-lasting Ca2+-activated K+ currents in rat visual cortex neurons.
【24h】

Brain-derived neurotrophic factor induces long-lasting Ca2+-activated K+ currents in rat visual cortex neurons.

机译：脑源性神经营养因子在大鼠视皮层神经元中诱导持久的Ca2 +激活的K +电流。

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

Brain-derived neurotrophic factor (BDNF) increases postsynaptic intracellular Ca2+ and modulates synaptic transmission in various types of neurons. Ca2+-activated K+ currents, opened mainly by intracellular Ca2+ elevation, contribute to hyperpolarization following action potentials and modulate synaptic transmission. We asked whether BDNF induces Ca2+-activated K+ currents by postsynaptic elevation of intracellular Ca2+ in acutely dissociated visual cortex neurons of rats. Currents were analysed using the nystatin-perforated patch clamp technique and imaging of intracellular Ca2+ mobilization with fura-2. At a holding potential of -50 mV, BDNF application (20 ng/mL) for 1-2 min induced an outward current (IBDNF-OUT; 80.0 +/- 29.0 pA) lasting for more than 90 min without attenuation in every neuron tested. K252a (200 nm), an inhibitor of Trk receptor tyrosine kinase, and U73122 (3 microm), a specific phospholipase C (PLC)-gamma inhibitor, suppressed IBDNF-OUT completely. IBDNF-OUT was both charybdotoxin- (600 nm) and apamin- (300 nm) sensitive, suggesting that this current was carried by Ca2+-activated K+ channels. BAPTA-AM (150 microm) gradually suppressed IBDNF-OUT. Fura-2 imaging revealed that a brief application of BDNF elicited a long-lasting elevation of intracellular Ca2+. These results show that BDNF induces long-lasting Ca2+-activated K+ currents by sustained intracellular Ca2+ elevation in rat visual cortex neurons. While BDNF, likely acting through the Trk B receptor, was necessary for the induction of long-lasting Ca2+-activated K+ currents via intracellular Ca2+ elevation, BDNF was not necessary for the maintenance of this current.
机译：脑源性神经营养因子（BDNF）增加突触后细胞内Ca2 +，并调节各种类型神经元中的突触传递。 Ca2 +激活的K +电流主要由细胞内Ca2 +升高打开，在动作电位后促进超极化并调节突触传递。我们问BDNF是否通过大鼠急性解离的视觉皮层神经元的细胞内Ca2 +的突触后升高来诱导Ca2 +激活的K +电流。使用制霉菌素穿孔的膜片钳技术分析电流，并使用fura-2对细胞内Ca2 +动员进行成像。在-50 mV的保持电势下，施加BDNF（20 ng / mL）1-2分钟会诱导持续90分钟以上的向外电流（IBDNF-OUT; 80.0 +/- 29.0 pA），而在每个测试的神经元中均无衰减。 Trk受体酪氨酸激酶抑制剂K252a（200 nm）和特定的磷脂酶C（PLC）-γ抑制剂U73122（3 microm）完全抑制了IBDNF-OUT。 IBDNF-OUT对Charybdotoxin-（600 nm）和Apamin-（300 nm）均敏感，表明该电流由Ca2 +激活的K +通道携带。 BAPTA-AM（150微米）逐渐抑制IBDNF-OUT。 Fura-2成像显示，BDNF的短暂应用引起细胞内Ca2 +的长期升高。这些结果表明，BDNF通过持续维持大鼠视皮层神经元内细胞内Ca2 +升高，诱导持久的Ca2 +激活的K +电流。虽然BDNF可能通过Trk B受体起作用，但对于通过细胞内Ca2 +升高诱导持久的Ca2 +激活的K +电流是必需的，而BDNF对于维持该电流不是必需的。

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