An increase in cyclin G expression after nerve injury was demonstrated by differential display PCR, carried out to compare references in expression of mRNAs between axotomized and normal hypoglossal motoneurons in the rat. The nerve injury dramatically upregulated the expression of cyclin G mRNA in the motoneurons during the early phase of the nerve regeneration process, suggesting an involvement of cyclin G in the early stage of nerve regeneration. In brain, in situ hybridization studies also demonstrated cyclin G expression in a restricted group of matured neurons, particularly in the telencephalon and the thalamus. This constitutive expression in mature neurons suggests that cyclin G may have a function different from other members of the cyclin group. In addition, although cyclin G has been shown to be a transcription target of p53, the upregulation of cyclin G in injured motoneurons, as well as the expression in the adult rat brain, was not affected in the p53-deficient mouse. These data suggest that the expression of cyclin G, at least in the nervous system, is not regulated by p53 predominantly, and that there may be alternative regulatory factors or pathways for cyclin G expression.