中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (7): 1013-1017.doi: 10.4103/1673-5374.160092

• 综述:神经损伤修复保护与再生 •    下一篇

神经元和神经胶质细胞中的连接蛋白:损伤与疾病的干预靶标?

  

  • 收稿日期:2015-05-14 出版日期:2015-07-24 发布日期:2015-07-24

Connexins in neurons and glia: targets for intervention in disease and injury

Keith B. Moore 1, John O’Brien 1, 2   

  1. 1 Richard S. Ruiz, M.D. Department of Ophthalmology & Visual Science, The University of Texas Health Science Center at Houston, TX, USA
    2 The University of Texas Graduate School of Biomedical Sciences, Houston, TX, USA
  • Received:2015-05-14 Online:2015-07-24 Published:2015-07-24
  • Contact: John O’Brien, Ph.D.,John.OBrien@uth.tmc.edu.
  • Supported by:

    This work is supported by NIH grant R01EY012857 (JO), the Frederic B. Asche endowment and Research to Prevent Blindness. KBM is supported by T32EY007024.

摘要:

整个中枢神经系统中的神经元和神经胶质细胞会通过间隙连接组织成网络。其中,神经胶质细胞有利于代谢平衡和细胞间沟通;而神经元,主要用于缝隙连接形成电突触的通信功能。然而,在神经退行性变条件下,由于疾病或损伤造成的间隙连接会对细胞存活造成损害。电突触可能有助于杀死神经元之间的过度活动和旁观者,而在神经胶质细胞中的间隙连接半通道可促进炎症信号及瘢痕形成。

Abstract:

Both neurons and glia throughout the central nervous system are organized into networks by gap junctions. Among glia, gap junctions facilitate metabolic homeostasis and intercellular communication. Among neurons, gap junctions form electrical synapses that function primarily for communication. However, in neurodegenerative states due to disease or injury gap junctions may be detrimental to survival. Electrical synapses may facilitate hyperactivity and bystander killing among neurons, while gap junction hemichannels in glia may facilitate inflammatory signaling and scar formation. Advances in understanding mechanisms of plasticity of electrical synapses and development of molecular therapeutics to target glial gap junctions and hemichannels offer new hope to pharmacologically limit neuronal degeneration and enhance recovery.

Key words: ischemia, retinal degeneration, amacrine cells, astrocytes, dopamine receptors, adenosine receptors, NMDA receptors, connexin mimetic peptides