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Editors Selection IGR 16-4

Basic research: BDNF and RGC

Comment by Yeni Yucel on:

21374 BDNF preserves the dendritic morphology of α- and β- ganglion cells in the cat retina after optic nerve injury, Weber AJ; Harman CD, Investigative Ophthalmology and Visual Science, 2008; 49: 2456-2463

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Following optic nerve injury, preservation of function and fine architecture of surviving RGCs is critical. Cell size and dendrite morphology are reliable correlates of the functional state of RGCs. RGC classification based on cell size and dendritic arbor pattern is relevant to RGC subtypes including alpha and beta types composing 60% of RGCs. It is possible to further characterize the RGCs as ON- and OFF-center, based on dendrite ramification in the inner plexiform layer. Assessing dendrite parameters in experimental models with candidate drugs may give valuable information on cell type-specific effects. Brain-derived neurotrophic factor (BDNF) has been shown to reduce RGC loss in mammalian retina following various optic nerve injuries. The original contribution of the work by Weber and Harman (809) is the demonstration that BDNF attenuates cell atrophy and dendrite pathology of RGCs following optic nerve crush injury. Experiments were performed in 18 adult cats with optic nerve crush. Nine received a single intraviteral injection of BDNF (30 μg and 90 μg) at the time of the optic nerve crush.

BDNF preserved the fi ne dendritic architecture of surviving RGCs after optic nerve crush injury

The remaining nine animals with optic crush received no treatment. Cell measurements from the fellow eye of the 18 experimental animals and from eyes of four normal animals were used as controls. Cell size and dendrite morphology were assessed the following seven days survival after optic crush injury. Intracellular labeling of the RGCs and their characterization were performed with state of the art techniques. This study clearly demonstrates the overall effects of BDNF on RGC dendrites. In the statistical analysis, soma and dendrite measurements were treated as independent observations and pooled for each experimental group. Mean values for each parameter in experimental and control groups were compared. Calculation of the mean RGC measurement per animal subject, followed by comparison of the mean of the means of the BDNF-treated optic nerve crush group compared to untreated optic nerve crush group might also have been helpful. This study clearly shows that BDNF preserved the fine dendritic architecture of surviving RGCs seven days after optic nerve crush injury. Further studies with longer survival times may shed new insights into the effect of BDNF on injured RGCs.

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