Transcriptional Activity of Nuclear Factor Kappa B (NF-κB) in Post-Traumatic Sensory Neurons (a histochemical study)

Nuclear factor kappa B (NF-κB) is a transcription factor that regulates the expression of a large set of genes involved in immune and inflammatory processes. It has been suggested that the release of specific cytokines following nerve damage has a stimulatory action, activating NF-κB in neurons in the spinal ganglia (SG), which may have protective influences on sensory neurons. However, the complexity of this factor has led to contradictory conclusions on the role of NF-κB in damaged SG neurons. The aim of the present work was to determine whether NF-κB is activated in sensory neurons in mature SG in conditions of peripheral nerve damage using transgenic reporter mice in which activation of NF-κB leads to expression of the lac-z reporter gene. These experiments showed that expression of β-galactosidase (β-gal) did not occur either in damaged SG neurons or in neurons on the contralateral side. However, powerful β-gal expression was seen in damaged muscle tissue. This may reflect the regressive influence of additional signal molecules on NF-κB activity in sensory neurons.