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Cell death in the inner nuclear layer of the retina is modulated by BDNF

Karen Cusato1, Alejandra Bosco, Rafael Linden

  • 1Instituto de Biofísica, UFRJ, CCS, bloco G, Cidade Universitária, Rio de Janeiro, 21949-900, Brazil.

Brain Research. Developmental Brain Research
|December 14, 2002
PubMed

Insights

Brain-derived neurotrophic factor (BDNF) influences the natural death of developing amacrine cells in the retina. Ganglion cells produce BDNF, which signals to amacrine cells via TrkB receptors.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Retinal Cell Biology

Background:

  • Developing amacrine cells in the vertebrate retina undergo programmed cell death.
  • Retinal ganglion cell (RGC) removal enhances this cell death.
  • BDNF is a neurotrophin implicated in neuronal survival and development.

Purpose of the Study:

  • To investigate the role of BDNF in regulating the naturally-occurring cell death of amacrine cells.
  • To determine if BDNF signaling is involved in the enhanced cell death observed after RGC removal.

Main Methods:

  • Whole-retina culture assay was used to study amacrine cell death.
  • BDNF was supplied exogenously to modulate cell death.
  • Soluble TrkB receptors were used to competitively inhibit endogenous BDNF signaling.

Main Results:

  • Modulating BDNF levels (either by addition or inhibition) altered the frequency of dying amacrine cells.
  • Retinal ganglion cells were identified as a source of BDNF.
  • Amacrine cells were shown to express TrkB receptors, the cognate receptors for BDNF.

Conclusions:

  • BDNF plays a significant role in regulating the survival of developing amacrine cells.
  • A signaling pathway involving BDNF produced by ganglion cells and acting on TrkB receptors of amacrine cells is proposed.
  • This pathway is critical for normal amacrine cell development and survival in the vertebrate retina.

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