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(Investigative Ophthalmology and Visual Science. 1974;13:771-783.)
© 1974 by The Association for Research in Vision and Ophthalmology, Inc.

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Effect of Intraocular Pressure on Rapid Axoplasmic Transport in Monkey Optic Nerve

DOUGLAS R. ANDERSON 1 and ANITA HENDRICKSON 1

1 Bascom Palmer Eye Institute, Department of Ophthalmology, University of Miami School of Medicine, Miami, Department of Ophthalmology, University of Washington School of Medicine, Seattle

Tritiated leucine was injected into the vitreous of owl monkeys (Aotus trivirgatus) to make it available to retinal ganglion cells for protein synthesis. Intraocular pressure was maintained for eight hours at selected levels between 15 and 105 mm. Hg. Autoradiography and scintillation counting were used to follow the movement of the labeled protein along the axons from the retinal ganglion cells to the lateral geniculate nucleus (LGN) by axoplasmic transport. At normal levels of intraocular pressure, label was distributed continuously along the retina, optic disc, and nerve, and radioactive label reached the LGN by eight hours. When the intraocular pressure was moderately elevated there was partial obstruction of axoplasmic transport in the region of the lamina cribrosa, but some label reached the optic nerve and LGN. When intraocular pressure was elevated to within 25 mm. Hg of mean blood pressure, there was complete obstruction of transport at the lamina cribrosa and label did not reach the LGN; retinal synthesis and transport along the axons to the optic nerve head continued. When the intraocular pressure approached or exceeded mean blood pressure, retinal synthesis stopped, as evidenced by absence of label in both the retina and disc. Our conclusions are that: (1) axoplasmic transport is affected by intraocular pressure, (2) there is a selective effect deep in the optic nerve head at the lamina cribrosa, and (3) a partial effect can be detected even at moderate elevations of intraocular pressure. Whether the obstruction is mechanical or is secondary to reduced blood flow has not been determined, and the exact relevance of these findings to the pathogenic mechanisms of glaucomatous cupping is not yet clear.

Note:
Presented at the David G. Cogan Symposium of the Association for Research in Vision and Ophthalmology, April 27, 1974, Sarasota, Fla.

Key Words: axoplasmic transport • glaucomatous cupping • intraocular pressure • experimental glaucoma.

Submitted on May 2, 1974




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