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Editors Selection IGR 9-1

Basic research: ET-1 effect on ON

Comment by George Cioffi on:

20794 Acute endothelin-1 application induces reversible fast axonal transport blockade in adult rat optic nerve, Wang X; Baldridge WH; Chauhan BC, Investigative Ophthalmology and Visual Science, 2008; 49: 961-967

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Endothelin-1 causes a reversible blockade of the fast component of the retrograde axoplasmic flow in the anterior optic nerve

Wang et al. (112) continue previous work from this laboratory with an elo-quent set of experiments examining the acute effects of Endothelin-1 (ET-1) on the anterior optic nerve. They exposed the optic nerve surface to ET-1 via a sponge delivery system at dosages (1 nM) that they had previously investigated. In this previous work, they showed that this level of acute ET-1 exposure did not result in significant global blood flow alterations with the anterior optic nerve. However, the present study demonstrates a reversible blockade of the fast component of the retrograde axoplasmic flow, as measured by horseradish peroxidase (HRP) techniques. Of particular interest is that the rapid axonal transport was arrested by two hours following the ET-1 exposure, but recovered fully by six hours. As well, there did not seem to be any significant damage to the optic nerve, as measured by retinal ganglion cell loss.

Endothelin-1 belongs to a family of peptides produced primarily from the vascular endothelium and has known vasoactive, as well as other physiological, effects. It is an extremely potent vasoconstrictor that plays a key role in the vasomotor status of the CNS and other end organs. ET-1 has been suggested to play a role in the development of glaucomatous optic neuropathy perhaps by creating localized blood flow deficiencies or by other mechanisms yet to be elucidated. The findings of this manuscript highlight another potential direct effect of ET-1 on the optic nerve that may contribute to the progressive loss of RGCs in glaucomatous optic neuropathy. However, further evidence is needed to demonstrate that these low levels of ET-1 are not altering axoplasmic flow via localized ischemia. The finding of a reversible component to this process is very exciting in that it offers a potential therapeutic target that may enhance optic nerve survival in patients with glaucoma.

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