June 1999
Volume 40, Issue 7
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Articles  |   June 1999
Effects of the neurotrophin brain-derived neurotrophic factor in an experimental model of retinal detachment.
Author Affiliations
  • G P Lewis
    Neuroscience Research Institute, University of California, Santa Barbara 93106, USA.
  • K A Linberg
    Neuroscience Research Institute, University of California, Santa Barbara 93106, USA.
  • S F Geller
    Neuroscience Research Institute, University of California, Santa Barbara 93106, USA.
  • C J Guérin
    Neuroscience Research Institute, University of California, Santa Barbara 93106, USA.
  • S K Fisher
    Neuroscience Research Institute, University of California, Santa Barbara 93106, USA.
Investigative Ophthalmology & Visual Science June 1999, Vol.40, 1530-1544. doi:
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    • Get Citation

      G P Lewis, K A Linberg, S F Geller, C J Guérin, S K Fisher; Effects of the neurotrophin brain-derived neurotrophic factor in an experimental model of retinal detachment.. Invest. Ophthalmol. Vis. Sci. 1999;40(7):1530-1544.

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

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Abstract

PURPOSE: To examine the effects of brain-derived neurotrophic factor (BDNF) in an animal model of retinal detachment. METHODS: Cat retinas were detached from the retinal pigment epithelium for either 7 or 28 days. Animals received either an intravitreal injection of BDNF (100 ILg) or phosphate-buffered saline (PBS), the vehicle for BDNF. Retinas were evaluated using morphology and immunocytochemistry. The width of the outer segment zone was measured, and the retinas were evaluated for changes in protein expression by labeling with antibodies to rod opsin, phosducin, synaptophysin, calbindin D, and glial fibrillary acidic protein (GFAP). The effect of BDNF on both proliferation and apoptotic cell death was examined. RESULTS: Although there was variability in the treated retinas, most of the animals receiving BDNF had well-organized outer segments that were longer than those in vehicle-treated controls. Immunocytochemistry revealed that treated retinas had consistently less opsin redistribution to the plasma membrane, less phosducin upregulation, and fewer calbindin D-labeled horizontal cell processes. BDNF did not reduce overall cell death in the detachments or death of photoreceptors by apoptosis. However, it significantly reduced the proliferative response of Miller cells and the extent of upregulation of GFAP. CONCLUSIONS. The results suggest that BDNF may aid in the recovery of the retina after reattachment by maintaining the surviving photoreceptor cells, by reducing the gliotic effects in Müller cells, and perhaps by promoting outer segment regeneration.

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