AbstractStudies employing axoplasmic transport techniques have suggested that the central arbors of vibrissae‐related primary afferents are rapidly and permanently lost from the trigeminal (V) brainstem complex after transection of the intraorbital nerve (ION). The present study reexamined this issue using immunocytochemistry for galanin (GAL) and anterograde labelling with Di‐I to evaluate V brainstem organization in rats that sustained damage to the ION or individual vibrissae follicles in infancy or adulthood. After adult nerve damage, GAL‐positive fibers are increased in layers I and II of V subnucleus caudalis (SpC). This was apparent by 3 days after the lesion. In rats that sustained nerve damage at birth (PO), GAL immunoreactivity (IR) appeared throughout the V brainstem complex and had a patchy distribution similar to that of vibrissae‐related V primary afferents in normal rats. Increased GAL‐IR in rostral portions of the V brainstem complex was observed in rats that sustained ION damage as late as P14. Additional experiments in which nerve damage was followed by destruction of the V ganglion demonstrated that this GAL‐IR was contained in primary afferents. Damage to single vibrissa follicles or to a row of follicles produced a single patch or row of GAL‐IR terminals in the somatotopically appropriate portion of the ipsilateral V brainstem complex. Di‐I labelling in neonatally nerve‐damaged rats demonstrated that primary afferent axons filled the central territory normally innervated by this nerve and that their terminal distribution was patchy. These results suggest that the V ganglion cells that survive neonatal axotomy may retain somatotopically organized projections to the V brainstem complex for at least a limited postnatal period.