Chick collapsin‐1, a member of the semaphorin family, has been implicated in axonal pathfinding as a repulsive guidance cue. Collapsin‐1 induces growth cone collapse via a pathway which may include CRMP‐62 and heterotrimeric G proteins. CRMP‐62 protein is related to UNC‐33, a nematode neuronal protein required for appropriately directed axonal extension. Mutations in unc‐33 affect neural microtubules, the basic cytoskeletal elements for axoplasmic transport. Using computer‐assisted video‐enhanced differential interference contrast microscopy, we now demonstrate that collapsin‐1 potently promotes axoplasmic transport. Collapsin‐1 doubles the number of antero‐ and retrograde‐transported organelles but not their velocity. Collapsin‐1 decreases the number of stationary organelles, suggesting that the fraction of time during which a particle is moving is increased. Collapsin‐1‐stimulated transport occurs by a mechanism distinct from that causing growth cone collapse. Pertussis toxin (PTX) but not its B oligomer blocks collapsin‐induced growth cone collapse. The holotoxin does not affect collapsin‐stimulated axoplasmic transport. Mastoparan and a myelin protein NI‐35 induce PTX‐sensitive growth cone collapse but do not stimulate axoplasmic transport. These results provide evidence that collapsin has a unique property to activate axonal vesicular transport systems. There are at least two distinct pathways through which collapsin exerts its actions in developing neurons. © 1997 John Wiley & Sons, Inc. J Neurobiol 33: 316–328, 1997