We report that: (1) An increase in the transcription activity is a mechanism by which trophic peptides may regulate the expression of PAC1. (2) An activation of the PAC1 promoter does not necessarily correlate with the neurotrophin-promoted neuritogenesis. (3) Activation of the PAC1 promoter is probably an early event since the EGF response is rather weak and transient in PC12 cells. (4) MAP kinase pathway activation is necessary for the NGF effect. The mechanism of the antagonism between PACAP and NGF observed on the PAC1 promoter activity and already described in regulating chromaffin cell proliferation, remains to be explained.