Initiation of fast axonal transport: involvement of calcium during transfer of proteins from Golgi apparatus to the transport system.

Fast axonal transport of [³H]fucose-labelled glycoproteins was examined in vitro in a preparation of spinal sensory neurons of the bullfrog. Rapidly transported glycoproteins were labelled when dorsal root ganglia were exposed to [³H]fucose, but not when a localized region of spinal nerve trunk was exposed to the labelled sugar; these results are consistent with the general finding that fucosylation occurs predominantly in the Golgi apparatus. Incubation of ganglia and nerve trunks in medium containing 0.18 mM CoCl₂ depressed the amount of rapidly transported, [³H]fucose-labelled glycoprotein by approximately 80%. This level of cobalt impairs neither protein synthesis nor incorporation of [³H]fucose into glycoprotein, suggesting that the inhibition of axonal transport by cobalt occurs at a step subsequent to fucosylation. When a 4 mm region of spinal nerve was desheathed, to facilitate access of ions to the axons, cobalt had no effect on fast axonal transport of glycoproteins at the level of the axon: the amount of [³H]fucose-labelled protein was similar in the regions of nerve trunk proximal and distal to the desheathed area.Thus, the cobalt-sensitive step in the transport of glycoproteins is likely to occur in the somata during transfer of the proteins from the Golgi apparatus to the transport system; it is suggested that cobalt antagonizes the action of intracellular calcium ions. An analogy is considered between the processing of fast-transported proteins by neuronal somata and the processing of secretory proteins by pancreatic exocrine cells.