Axonal transport and transneuronal transfer in mouse visual system following injection of [3H]fucose into the eye
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After the injection of [3H]fucose into the mouse eye, the axonal transport of radioactive glycoproteins to the lateral geniculate body and superior colliculus showed two phases: The early phase of transported radioactivity, which was more prominent, rose to a peak at 24 to 48 h after the injection and then decayed to about half its maximum value over the next 2 to 3 days; this was followed by the late phase, consisting of a plateau or shallow rise lasting until 2 to 3 weeks after the injection and then decaying with a half-time of about 2 weeks. The early phase could be attributed to the arrival of glycoproteins carried by the fast component of axonal transport. The late phase was not due to slow transport but was probably generated by the fast transport of some glycoproteins that were slowly released from the cell body. Transneuronally transferred radioactivity appearing in the striate cortex and retrosplenial cortex similarly showed two phases. If the injected eye was removed 4 h after the fucose injection, preventing the further entry of transportable material into the optic axons, both the axonally transported and transneuronally transferred radioactivity in the early phase were reduced by about 60%, and the late phase of axonal transport was abolished; the transneuronally transferred material normally appearing in the late phase was either eliminated or greatly reduced. If the enucleation was performed 2 days after the injection, the early phase of axonal transport declined with its normal time course for several days and then with a linear time course for 4 to 5 weeks. This rate of disappearance of radioactivity was much slower than in comparable experiments in which [3H]proline was used as precursor. Although the late phase of axonal transport of glycoproteins did not appear in the enucleated animals, the transneuronally transferred material did show a late phase, which was of normal magnitude in the retrosplenial cortex, though possibly somewhat reduced in the striate cortex. Therefore the transneuronally transferred material appearing at the same time as the late phase of axonal transport must have been derived from material reaching the axon terminals in the early phase. These results are consistent with the hypothesis that both in the cell body and in the axon terminals the fucosyl glycoproteins are distributed in a rapid-release pool as well as a slow-release pool. Material released from either pool in the cell body is delivered by fast axonal transport to the corresponding pool in the axon terminals, and both pools in the terminals serve as sources for transneuronally transferred material. However, since the slow-release pool in the terminals also receives material from the rapid-release pool, the slow-release pool can provide material for trans-neuronal transfer even when the late phase of axonal transport has been abolished by axotomy. It is possible that at the axon terminals the slow-release pool is located in the glial cells. © 1977.
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