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Kazuhito Ikeda, Hidenobu Tanihara, Yoshihito Honda, Tohru Tatsuno, Hiroshi Noguchi, Chikao Nakayama; BDNF Attenuates Retinal Cell Death Caused by Chemically Induced Hypoxia in Rats. Invest. Ophthalmol. Vis. Sci. 1999;40(9):2130-2140.
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purpose. To investigate the neuroprotective effects of brain-derived
neurotrophic factor (BDNF) against potassium cyanide (KCN)–induced
methods. Rats were injected intravitreally with iodinated BDNF. Two days later,
eyeballs were dissected into various parts, and the level of
radioactivity in each part was measured. Retinal damage was induced by
incubating rat eyeballs with 5 mM KCN. BDNF was injected intravitreally
2 days before KCN treatment, and subsequent morphometric analysis was
carried out to evaluate the retinal cell damage. To elucidate the
mechanisms of BDNF’s neuroprotective effects, the intravitreal
concentrations of amino acids and the expression of calretinin were
results. Intravitreally injected BDNF was distributed evenly throughout the
eyes, and the incorporation of iodinated BDNF into the retina was three
times higher than in other ocular tissues. Immunohistochemical analysis
demonstrated that exogenous BDNF diffused throughout the retina and was
especially concentrated in the inner (INL) and outer nuclear layer.
Morphometric analysis showed that the number of INL cells of the
posterior area, 880 μm from the optic nerve head, was 190 ± 4
with KCN treatment and 284 ± 9 in control animals. Cell death
appeared to be necrotic. When eyes injected with either
phosphate-buffered saline (PBS) or BDNF were subjected to treatment
with KCN, the number of INL cells was 186 ± 5 in the PBS-treated
controls and 253 ± 8 in eyes treated with BDNF. Also, BDNF
increased the number of calretinin-positive cells in the INL and
reduced the KCN-induced elevation of intravitreal glutamate levels.
conclusions. BDNF injected intravitreally reaches the retina and attenuates the INL
cell death caused by KCN-induced metabolic insult. The neuroprotective
effects of BDNF are partly ascribed to the upregulation of a
calcium-binding protein and the attenuation of glutamate release into
the vitreous body.
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