The effects of prostaglandin E2 on axonal transport in cultured mouse dorsal root ganglion neurons were investigated by analysing the number of axonally transported particles under video-enhanced microscopy. Application of prostaglandin E2 increased the number of particles transported in anterograde and retrograde directions. The EP2 prostaglandin receptor agonist butaprost mimicked the effect of prostaglandin E2, but the EP1/EP3 prostaglandin receptor agonist 17-phenyl trinor prostaglandin E2 and the EP3 prostaglandin receptor agonist M and B 28767 had no effect. The membrane-permeable cyclic AMP analogue dibutyryl cyclic AMP and the adenylate cyclase activator forskolin mimicked the effect of prostaglandin E2. The protein kinase A inhibitor H-89 reversibly reduced the number of particles in both anterograde and retrograde directions. The effects of prostaglandin E2 and dibutyryl cyclic AMP were blocked by H-89. Taken together with previous biochemical studies showing that prostaglandin E2 increases cyclic AMP levels, the present results suggest that prostaglandin E2 enhances axonal transport via the EP2 receptor and cyclic AMP-dependent protein kinase A pathway. We further investigated the role of prostaglandin E2 in neurite growth. Prostaglandin E2 increased both the number of cells exhibiting neurites and the neurite growth rate, operating by a similar mechanism to stimulation of axonal transport.Prostaglandin E2 may modulate axonal transport to supply materials for morphogenesis as well as other functions in sensory neurons. Copyright (C) 2000 IBRO.