March 1979

Blockade of Rapid Axonal TransportEffect of Intraocular Pressure Elevation in Primate Optic Nerve

Author Affiliations

From the Glaucoma Service, Wilmer Institute, Johns Hopkins University School of Medicine, Baltimore (Dr Quigley), and the William L. McKnight Vision Research Center, Bascom Palmer Eye Institute, Department of Ophthalmology, University of Miami School of Medicine (Drs Guy and Anderson).

Arch Ophthalmol. 1979;97(3):525-531. doi:10.1001/archopht.1979.01020010269018

• After acute intraocular pressure (IOP) elevation, an induced disturbance of rapid axonal transport at the optic nerve head began within three hours at the IOP levels tested. The accumulation of radioactive label at the scleral lamina cribrosa increased with time of IOP elevation. There was a 60% decrease in the amount of transported material in the optic nerve, tract, and lateral geniculate body (LGN). Detailed analysis suggests that this decrease is not due to a simple slowdown of transport, but results from a total block of rapid transport in some axons, with no impairment in other axons. This total blockade of rapid transport by elevated IOP in involved axons differs from the apparent slowdown of transport in experimental papilledema, and the difference may explain the response of ganglion cells to the two conditions.