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Mary Ellen Pease, Stuart J. McKinnon, Harry A. Quigley, Lisa A. Kerrigan–Baumrind, Donald J. Zack; Obstructed Axonal Transport of BDNF and Its Receptor TrkB in Experimental Glaucoma. Invest. Ophthalmol. Vis. Sci. 2000;41(3):764-774.
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purpose. In both animal model systems and in human glaucoma, retinal ganglion
cells (RGCs) die by apoptosis. To understand how RGC apoptosis is
initiated in these systems, the authors studied RGC neurotrophin
transport in experimental glaucoma using acute intraocular pressure
(IOP) elevations in rats and chronic IOP elevation and unilateral optic
nerve transections in monkeys.
methods. Eyes were studied in masked fashion by light and electron microscopy
and by immunohistochemistry with antibodies directed against the
tyrosine kinase receptors (TrkA, B, and C) and against brain-derived
neurotrophic factor (BDNF), as well as by autoradiography to identify
retrograde axonal transport of 125I-BDNF injected into the
results. With acute glaucoma in the rat, RGC axons became abnormally dilated,
accumulating vesicles presumed to be moving in axonal transport at the
optic nerve head. Label for TrkB, but not TrkA, was relatively
increased at and behind the optic nerve head with IOP elevation.
Abnormal, focal labeling for TrkB and BDNF was identified in axons of
monkey optic nerve heads with chronic glaucoma. With acute IOP
elevation in rats, radiolabeled BDNF arrived at cells in the RGC layer
at less than half the level of control eyes.
conclusions. Interruption of BDNF retrograde transport and accumulation of TrkB at
the optic nerve head in acute and chronic glaucoma models suggest a
role for neurotrophin deprivation in the pathogenesis of RGC death in
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