April 2009
Volume 50, Issue 13
ARVO Annual Meeting Abstract  |   April 2009
Degeneration of Beta Ganglion Cells in Development Leads to Selective Death of Cells in the Inner Nuclear Layer
Author Affiliations & Notes
  • M. A. MacNeil
    Biology, York College CUNY, Jamaica, New York
    Biology, Graduate Center of CUNY, New York, New York
  • S. Purrier
    Biology, York College CUNY, Jamaica, New York
  • R. J. Rushmore
    Anatomy and Neurobiology, Boston University School of Medicine, Boston, Massachusetts
  • Footnotes
    Commercial Relationships  M.A. MacNeil, None; S. Purrier, None; R.J. Rushmore, None.
  • Footnotes
    Support  NIH Grants GM08153, NS33975, and PSC-CUNY Grant 61371-00-39
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 5688. doi:
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    • Get Citation

      M. A. MacNeil, S. Purrier, R. J. Rushmore; Degeneration of Beta Ganglion Cells in Development Leads to Selective Death of Cells in the Inner Nuclear Layer. Invest. Ophthalmol. Vis. Sci. 2009;50(13):5688.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Damage to primary visual cortex early in life results in the death of 90% of beta retinal ganglion cells in the cat retina. The purpose of this study was to test whether the selective death of these cells leads to reorganization of the inner nuclear layer.

Methods: : Retinas from normal cats and from animals that had primary visual cortical areas 17 and 18 removed on the day of birth (P1) were embedded in plastic and serially sectioned with an ultramicrotome. The sections were imaged, all cells in the images identified according to class, counted and the ratios of ganglion, amacrine, bipolar, Müller and horizontal cells determined. For analysis of cell populations, sections from both retinas were labeled with antibodies against protein kinase C (PKC), GABA, choline acetyltransferase (ChAT) and calretinin and counterstained with ethidum homodimer.

Results: : The early lesions of visual cortex resulted in the death of nearly all ganglion cells with medium-sized somas, but did not disrupt the general composition of the INL or the thickness of the IPL; cell densities within the INL were similar in both groups. Counts of the cells in the INL revealed that the overall fractions of bipolar cells were higher in P1 lesion retinas compared to intact controls (64% vs. 62%) and amacrine cells showed a corresponding drop (19% vs. 21%). Müller and horizontal cells showed no change in relative proportions between the groups (15% and 1% respectively). There were no significant differences between the retinas when stained for ChAT, indicating that some cell classes were unaffected by the death of beta ganglion cells. However, in the P1 lesion retinas, we noted a significant decrease in the numbers of GABA-stained amacrine cells and a significant increase in the fractions of cells stained for PKC and calretinin. In intact retinas, PKC-stained rod bipolar cells made up 72% of all bipolar cells, but after the death of beta ganglion cells, the fraction of rod bipolar cells increased to 84%. This suggests that as many as 40% of cone bipolar cells died following the death of beta ganglion cells.

Conclusions: : Our results suggest that normal development of cells in the INL depends in part on the availability of normal post-synaptic targets. Understanding the factors that affect the survival and death of neurons in the retina may help us to understand how to rescue cells vulnerable to target removal caused by injury or disease.

Keywords: bipolar cells • development • amacrine cells 

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