Inhibition of nuclear factor-κB impairs reconsolidation of morphine reward memory in rats.

Drug addiction is a process associated with synaptic plasticity in which a drug of abuse affects the midbrain limbic system. Previous studies have indicated that drug abuse can be inhibited by disrupting the reconsolidation of a drug-related memory. Nuclear factor-κB (NF-κB) plays an important role in modulating different stages of memory, including reconsolidation, but its role in the reconsolidation of a reward memory has not been investigated. The aim of the present study was to examine the role of NF-κB in drug-related memory reconsolidation. We found that rats acquired morphine-induced conditioned place preference, which was inhibited by the NF-κB inhibitor SN50 administered after reexposure to a previously morphine-paired chamber (i.e., a memory retrieval process). The disruptive effect of SN50 on reward memory reconsolidation was reversed by systemic injections of the histone deacetylase inhibitor sodium butyrate. These results indicate that SN50 disrupts morphine-related memory reconsolidation by inhibiting NF-κB, and this effect can be reversed by inhibiting histone acetylation.