The expression of galanin and neuropeptide Y (NPY) by primary afferent neurons, including those in the trigeminal (V) system, is markedly up-regulated after peripheral nerve damage and might be expected to influence the response of central somatosensory cells to such damage. In the present study, we assessed the effects of four manipulations that have been used to study development and maintenance of vibrissae-related patterns in the V system-nerve transection, whisker clipping, activity blockade with tetrodotoxin (TTX), and axoplasmic transport attenuation with vinblastine-upon the expression of galanin and NPY by V ganglion cells and their central axons in the V brainstem complex. Both neonatal transection of the infraorbital nerve (ION) and application of vinblastine to it resulted in a marked up-regulation of galanin and NPY in V ganglion cells and their central axon arbors in animals killed on postnatal day 6. Neither whisker clipping nor application of TTX to the ION produced such changes. Both ION transection and application of vinblastine to this nerve resulted in a loss of vibrissae-related cellular patterns in the brainstem, but TTX application and whisker clipping did not. These results raise the possibility that up-regulation of galanin and NPY may play a role in the disappearance of vibrissae-related cellular patterns in the brainstem of rats that sustain neonatal ION damage.