National Institute on Drug Dependence, Peking University, Beijing 100191, China.
Behav Brain Res. 2011 Jan 20;216(2):592-6. doi: 10.1016/j.bbr.2010.08.047. Epub 2010 Sep 15.
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.
药物成瘾是一种与突触可塑性相关的过程，其中滥用药物会影响中脑边缘系统。先前的研究表明，通过破坏与药物相关的记忆的再巩固，可以抑制药物滥用。核因子-κB（NF-κB）在调节记忆的不同阶段（包括再巩固）中起着重要作用，但它在奖励记忆的再巩固中的作用尚未得到研究。本研究旨在探讨 NF-κB 在与药物相关的记忆再巩固中的作用。我们发现，大鼠获得了吗啡诱导的条件性位置偏好，而在重新暴露于先前与吗啡配对的室后给予 NF-κB 抑制剂 SN50（即记忆检索过程）可以抑制这种偏好。全身性注射组蛋白去乙酰化酶抑制剂丁酸钠可逆转 SN50 对奖励记忆再巩固的破坏作用。这些结果表明，SN50 通过抑制 NF-κB 破坏吗啡相关记忆的再巩固，而通过抑制组蛋白乙酰化可以逆转这种作用。
