Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (9): 1376-1378.doi: 10.4103/1673-5374.165224

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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.

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.