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

作　　者：Keith B.Moore John O'Brien 

机构地区：[1]Richard S.Ruiz, M.D.Department of Ophthalmology & Visual Science, The University of Texas Health Science Center at Houston [2]The University of Texas Graduate School of Biomedical Sciences

出　　处：《Neural Regeneration Research》2015年第7期1013-1017,共5页中国神经再生研究（英文版）

基　　金：supported by NIH grant R01EY012857(JO);the Frederic B.Asche endowment and Research to Prevent Blindness.KBM is supported by T32EY007024

摘　　要：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.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.

关 键 词：ischemia retinal degeneration amacrine cells astrocytes dopamine receptors adenosine receptors NMDA receptors connexin mimetic peptides 

分 类 号：R741[医药卫生—神经病学与精神病学]