中国神经再生研究(英文版) ›› 2015, Vol. 10 ›› Issue (9): 1376-1378.doi: 10.4103/1673-5374.165224

• 观点:视神经损伤修复保护与再生 • 上一篇    下一篇

穆勒细胞可塑性与再生:在脊椎动物视网膜中的验证

  

  • 收稿日期:2015-06-16 出版日期:2015-09-28 发布日期:2015-09-28

Neurochemical plasticity of Müller cells after retinal injury: overexpression of GAT-3 may potentiate excitotoxicity

Clarissa S. Schitine, Fernando G. de Mello, Ricardo A.M. Reis   

  1. Laboratório de Neuroquímica, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21941-902, Brazil (Schitine CS, de Mello FG, Reis RAM)
    Laboratório de Neuroanatomia Celular, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ 21941-902, Brazil (Schitine CS)
  • Received:2015-06-16 Online:2015-09-28 Published:2015-09-28
  • Contact: Ricardo A.M. Reis, Ph.D., ramreis@biof.ufrj.br.

摘要:

视网膜是一种从中央到外围梯度的多层组织。它的结构来源于多能前体,通过视网膜细胞系的克隆分析,这些祖细胞会生成不同的细胞类型,并被复杂的内在和外在因素的影响控制。
几种类型的神经元和一个主神经胶质细胞以一个高度有组织的方式构成脊椎动物视网膜。米勒细胞是视网膜和最后细胞类型分化的主要神经胶质细胞。一旦损坏或在生长因子刺激的影响下,它们会增殖,脱分化并且可以成为不同脊椎动物视网膜新神经元再生的来源。最近的数据表明,由兴奋毒性损伤诱导的视网膜体内病可由降低的抑制性强直性痉挛增效,因为米勒细胞细胞的GAT-3过表达会引起GABA摄取增加。并且进一步的研究也是是必要的,用来揭示参与谷氨酸依赖性GAT-3质膜级降低的分子机制。然而有趣的是,他们的观察开启了使用GABA转运抑制剂防止视网膜神经节细胞退变的新方式,并通过遵循视网膜退变最终达到反应性神经胶质增生的可能性

Abstract:

The retina is a multilayered tissue that develops following a central-to-peripheral gradient. Its structure derives from multipotent precursors, as shown through clonal analysis of retinal cells lineage. These progenitors generate diverse cell types, controlled by complex influences of intrinsic and extrinsic factors.
Several types of neurons and one main glia cell constitute the vertebrate retina, constructed in a highly organized manner. Müller cell is the predominant glia of the retina and the last cell type to differentiate. Upon damage or under the influence of growth factors stimulation, they proliferate, de-differentiate and can become a source of new neurons for retina regeneration in different vertebrates. The recent data suggest that in vivo lesions of the retina induced by excitotoxic insults may be potentiated by decreased inhibitory tonus, due to increased GABA uptake by Müller cells overexpressing GAT-3. Further investigations are necessary to reveal the molecular mechanisms involved in glutamate-dependent GAT-3 plasma membrane level reduction. Interestingly however, their observations open the possibility of using GABA transport inhibitors to prevent RGCs degeneration eventually caused by reactive gliosis that follow retina degeneration.