Several observations including NF-κB activation by glutamate, cytokines and oxidative stress, ability to transmit signals from the cytoplasm and synapses to the cell nuclei and regulation of synaptic plasticity and neuron survival [15], [16], [22], [25]–[29], suggest a role of this transcription factor in adaptation to chronic alcohol intake. Induction of oxidative stress by alcohol and alcoholism-associated alterations in the expression of inflammatory, cell survival and myelin genes [12]–[14] regulated by NF-κB [15]–[17], [32], [33] support this hypothesis. In the present study, we aimed to evaluate whether the NF-κB system is involved in neuroadaptation of the human brain to chronic alcohol abuse. The PFC involved in alcohol dependence and cognitive behavior, and impaired in human chronic alcoholics was chosen for analysis. The motor cortex (MC) that is not engaged in these processes to the same extent and is less affected by alcohol with respect to neuronal density [8], [10], was studied for comparison. The NF-κB system was characterized with biochemical and molecular techniques, and the alterations found were correlated with changes in the pattern of gene expression previously identified in the PFC of human chronic alcoholics [14].
