中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (10): 1537-1539.doi: 10.4103/1673-5374.165215

• 综述:神经损伤修复保护与再生 • 上一篇    下一篇

设置治疗神经可塑性的门槛:缺血长时程增强

  

  • 收稿日期:2015-07-30 出版日期:2015-10-28 发布日期:2015-10-28
  • 基金资助:

    这项工作由德国以色列基金会(G-1317-418.13/2015)支持

Ischemic long-term-potentiation (iLTP): perspectives to set the threshold of neural plasticity toward therapy

Maximilian Lenz1, 2, Andreas Vlachos2, Nicola Maggio1, 3, *   

  1. 1 Department of Neurology, The J. Sagol Neuroscience Center, The Chaim Sheba Medical Center, Tel HaShomer, Israel
    2 Institute of Clinical Neuroanatomy, Neuroscience Center Frankfurt, Goethe-University Frankfurt, Frankfurt, Germany
    3 Talpiot Medical Leadership Program, The Chaim Sheba Medical Center, Tel HaShomer, Israel
  • Received:2015-07-30 Online:2015-10-28 Published:2015-10-28
  • Contact: Nicola Maggio, M.D., Ph.D.,nicola.maggio@sheba.health.gov.il.
  • Supported by:

    This work was supported by German Israeli Foundation (G-1317-418.13/2015 to AV and NM)

摘要:

虽然目前广为接受的观点是神经元表达可塑性能力的改变对神经系统的疾病过程起着重要作用,但病理状态下的神经可塑性仍然不能被很好地理解。而缺血性脑卒中是神经系统疾病中致残和死亡的主要原因,对医疗保健和社会经济负担也造成大的影响。对其中能够改善生存条件和部分或间接影响神经网络的神经可塑性研究结果仍然较少。我们根据最近的实验证据,表明病理学刺激是可以诱导突触可塑性的,即兴奋性突触的缺血性长时程增强,可通过影响存活神经元的网络重组,可能在脑卒中后康复发挥着重要作用。

Abstract:

The precise role of neural plasticity under pathological conditions remains not well understood. It appears to be well accepted, however, that changes in the ability of neurons to express plasticity accompany neurological diseases. Here, we discuss recent experimental evidence, which suggests that synaptic plasticity induced by a pathological stimulus, i.e., ischemic long-term-potentiation (iLTP) of excitatory synapses, could play an important role for post-stroke recovery by influencing the post-lesional reorganization of surviving neuronal networks.

Key words: ischemic LTP (iLTP, stroke, neural repair, synaptic plasticity, neural homeostasis