Abstract
Developing amacrine cells in the vertebrate retina undergo naturally-occurring cell death which is accentuated by the early removal of retinal ganglion cells. We show that providing BDNF or decreasing endogenous BDNF via competitive binding with soluble TrkB receptors in a whole-retina culture assay modulates the frequency of dying cells in the amacrine cell layer. Ganglion cells synthesize BDNF, and amacrine cells express TrkB receptors, suggesting a likely signaling mechanism.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Aging / metabolism
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Amacrine Cells / cytology
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Amacrine Cells / drug effects
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Amacrine Cells / metabolism*
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Animals
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Animals, Newborn
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Binding, Competitive / drug effects
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Binding, Competitive / physiology
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Brain-Derived Neurotrophic Factor / drug effects
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Brain-Derived Neurotrophic Factor / metabolism*
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Cell Count
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Cell Death / drug effects
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Cell Death / physiology*
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Cell Differentiation / drug effects
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Cell Differentiation / physiology*
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Cell Survival / drug effects
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Cell Survival / physiology
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Organ Culture Techniques
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Rats
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Rats, Inbred Strains
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Receptor, trkB / drug effects
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Receptor, trkB / metabolism*
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Retina / cytology
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Retina / growth & development*
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Retina / metabolism
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Retinal Ganglion Cells / cytology
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Retinal Ganglion Cells / drug effects
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Retinal Ganglion Cells / metabolism*
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Signal Transduction / drug effects
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Signal Transduction / physiology
Substances
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Brain-Derived Neurotrophic Factor
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Receptor, trkB