This study evaluated the effects of neonatal attenuation of axoplasmic transport in the infraorbital nerve (ION) on the organization of vibrissae-related patterns in the rat's CNS. Application of colchicine- or vinblastine- impregnated implants to the ION from birth until postnatal day (P)6 to P10 resulted in a 92.4% reduction in the number of trigeminal (V) ganglion cells labelled by application of horseradish peroxidase to the vibrissa pad and a 44.8% decrease in the number of Nissl-stained ganglion cells in the ophthalamic-maxillary portion of the V ganglion. These implants also decreased the number of myelinated fibres in the ION. In normal rats killed on P6-10, there was an average of 10273 +/- 1259 myelinated axons in the nerve. In the animals with colchicine- or vinblastine-treated implants, this value was 3891 +/- 1965. The highest axon count in an experimental animal was 9859. In all animals, axoplasmic transport attenuation resulted in the disappearance of normal vibrissae-related cytochrome oxidase patterns in the brainstem, thalamus and primary somatosensory cortex. Axoplasmic transport attenuation did not result in the disappearance of vibrissae-related ordering of V primary afferent terminal arbors, as demonstrated by anterograde labelling with neurobiotin. These results suggest that some factor conveyed from the periphery of the V ganglion and perhaps on to the brainstem is necessary for the maintenance of vibrissae-related patterns in the thalamus and cortex.