Nuclear factor kappa B (NFkappaB) is a ubiquitous nuclear transcription factor that regulates the expression of a number of genes involved in cell survival, immune and inflammatory processes. It has been hypothesized that after nerve injury, the release of specific cytokines may provide a stimulus for activation of the transcription factor NF-kappaB in adult dorsal root ganglia (DRG) neurons exerting the protective effect on the sensory neurons. However, the complexity of this transcription factor has led to some misleading conclusions about NF-kappaB signalling in injured DRG neurons. The goal of the present study is to find out whether NF-kappaB is involved in the transcriptional regulation of genes in adult primary sensory neurons after peripheral nerve transection. In this series of experiments, we used a transgenic line of NF-kappaB reporter mice in which activation of NF-kappaB drives the expression of the lac-z gene. We show that the expression of beta-galactasidase (beta-gal) is not detected in injured DRG neurons and contralateral neurons. However, a strong beta-gal expression was detected in the muscle at the injury site. It may reflect the repressive influence of additional signalling cascades on NF-kappaB activity in sensory neurons.