The distribution of immunoreactivity for neural cell adhesion molecule (NCAM) has been characterized during the formation of the trigeminal ganglion and during the process of axon outgrowth and target differentiation in the maxillary nerve-whisker system, in rat fetuses of known gestational age. Proliferating cells within the trigeminal placode are NCAM immunoreactive when first observed on embryonic day (E) 10. NCAM immunoreactivity is lost from placode-derived cells as they migrate to the trigeminal ganglion. It re-appears on ganglion cell somata and on centrally and peripherally projecting axons at the time of neurite outgrowth. NCAM-immunoreactive centrally projecting axons reach the developing brain stem two days before peripheral axons encounter the presumptive whisker pad. NCAM immunoreactivity on axons and somata is down regulated after P0, following target contact and whisker follicle differentiation. The presumptive dermis of the whisker pad at E13 appears as a sheet-like condensation of intensely NCAM immunostained cells. Discrete infraorbital row nerves can be identified on E13. These form in the subdermal region which contains only low levels of NCAM immunoreactivity. Condensations of NCAM immunostained mesenchyme replace the dermal sheet on E14 and each condensation is associated with a plexus of infraorbital nerve fibers. The epithelium overlying each condensation grows downward on E15. Focal epithelial regions become NCAM immunoreactive by E18. NCAM immunostaining within epithelial components of the whisker follicle is temporally correlated with contact by NCAM-immunoreactive infraorbital nerve fibers. The site restricted expression of NCAM immunoreactivity during trigeminal embryogenesis is consistent with the idea that NCAM plays an integral role in critical aspects of pattern formation in the maxillary nerve-whisker system, particularly in the organization of placode and non-placode derived trigeminal neuroblasts, axon outgrowth and in the differentiation of the vibrissae follicles.