TRANSCRIPTIONAL ACTIVITY OF NUCLEAR FACTOR KAPPA B (NFκB) IN POSTTRA UMATIC SENSORY NEURONS (HISTOCHEMICAL STUDY)
Nuclear factor kappa B (NFκB) 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-κB 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-κB signalling in injured DRG neurons. The goal of the present study is to find out whether NF-κB 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-κB reporter mice in which activation of NF-κB drives the expression of the <i>lac-z</i> gene. We show that the expression of β-galactasidase (β-gal) is not detected in injured DRG neurons and contralateral neurons. However, a strong β-gal expression was detected in the muscle at the injury site. It may reflect the repressive influence of additional signalling cascades on NF-κB activity in sensory neurons.