FAST AXONAL-TRANSPORT IN EARLY EXPERIMENTAL DISK EDEMA

  • 1 January 1980
    • journal article
    • research article
    • Vol. 19  (2) , 158-168
Abstract
Impairment of slow axonal transport in papilledema was previously documented, but the abnormalities in rapid transport were less certain. Fast axonal transport was studied in 19 primate eyes [Aotus trivirgatus and Macaca mulatta] subjected to ocular hypotomy for 6-72 h following surgical fistulization of the anterior chamber. Mild, irregular alterations in fast axonal transport were detected only after nerve head swelling. These changes in fast transport mechanisms in nerve head edema occur after, and may be secondary to, impaired slow axoplasmic flow and the resultant axonal swelling. Since prolonged complete interruption of axonal transport is theoretically inconsistent with the continued normal neuron function characteristic of papilledema, and previous data show a slowdown rather than a complete blockade of axonal transport in papilledema, in eyes with papilledema a complete block of axonal transport probably does not exist. The swelling apparently results when slow axoplasmic flow is locally slowed down but not totally stopped, with the axon distention producing secondary mild, irregular changes in fast axonal transport.

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