Plastic change occurs in the adult rat barrel receptor complex following peripheral deafferentation by removal of facial vibrissae (vibrissectomy) and can be prevented by prior depletion of brain norepinephrine. Growth-associated protein (GAP-43, B50, F1, pp46), a marker for synaptic reorganization, increases in the barrel cortex of adult rats following both peripheral and central deafferentation. Here we followed changes in GAP-43 mRNA expression in the barrel receptor system following vibrissectomy. Adult rats had unilateral total vibrissectomy with sparing of the central (C3) vibrissa. By in situ hybridization, GAP-43 mRNA first increased at 24h (9%, P < 0.05) in the ipsilateral trigeminal complex. Levels remained elevated (up to 25% of the unlesioned side) over the next 6 days, decreased to 88% at 7 days and returned to control levels at 14 days. Contralateral barrel cortex levels of GAP-43 mRNA increased by 14% at 4–5 days remained elevated through 7 days and returned to control levels by 14 days. Increased GAP-43 mRNA levels 6 days after vibrissectomy were reproduced by complete transection of the infraorbital nerve and were blocked by depletion of brain norepinephrine. No change occurred in ventrobasal thalamus GAP-43 mRNA at any time. Dot blot and Northern blot hybridizations of GAP-43 mRNA after vibrissectomy showed a 43% increase in the ipsilateral trigeminal complex and a 16% increase in the contralateral barrel cortex at 3 days and an 84% increase in ipsilateral trigeminal and 50% increase in contralateral barrel cortex GAP-43 mRNA at 6 days, respectively. Thus, deafferentation-induced plasticity in the barrel pathway depends upon norepinephrine and is associated with increase in both GAP-43 mRNA and protein suggesting that this may involve a structural change.