Programmed cell death of retinal cone bipolar cells is independent of afferent or target control

Patrick W Keeley1, Nils R Madsen1, Ace J St John1

  • 1Neuroscience Research Institute, University of California at Santa Barbara, Santa Barbara, CA 93106-5060, USA.

Developmental Biology
|August 30, 2014
PubMed

Insights

Programmed cell death in the developing nervous system is crucial for development. Cone bipolar cell death appears to be regulated intrinsically, not by synaptic partners.

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Programmed cell death is essential for nervous system development and histogenesis.
  • Synaptogenesis involves interactions with afferent and target cells modulating cell survival.
  • Cone bipolar cells are a specific neuronal population that undergoes developmental cell death.

Purpose of the Study:

  • To investigate the factors modulating programmed cell death in cone bipolar cells during development.
  • To determine if cell-intrinsic or extrinsic factors regulate cone bipolar cell survival.

Main Methods:

  • Utilized knockout models to study the role of the pro-apoptotic Bax gene.
  • Manipulated cone afferent populations to assess their impact on cone bipolar cell survival.
  • Altered retinal ganglion cell populations to examine their influence on cone bipolar cell numbers.

Main Results:

  • Knocking out the pro-apoptotic Bax gene significantly increased the numbers of three cone bipolar cell types.
  • Selective elimination of cone afferents did not alter cone bipolar cell numbers.
  • Increasing retinal ganglion cell populations did not affect cone bipolar cell numbers.

Conclusions:

  • Programmed cell death in cone bipolar cells is primarily regulated by cell-intrinsic mechanisms.
  • Interactions with synaptic partners, such as cone afferents and retinal ganglion cells, do not appear to modulate cone bipolar cell death.
  • Findings suggest a novel intrinsic pathway controlling neuronal cell death during development.

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