Tianjin Medical University, Tianjin, China.
PLoS One. 2012;7(6):e39696. doi: 10.1371/journal.pone.0039696. Epub 2012 Jun 26.
The inhibitor κB protein kinase/nuclear factor κB (IKK/NF-κB) signaling pathway is critical for synaptic plasticity. However, the role of IKK/NF-κB in drug withdrawal-associated conditioned place aversion (CPA) memory is unknown. Here, we showed that inhibition of IKK/NF-κB by sulphasalazine (SSZ; 10 mM, i.c.v.) selectively blocked the extinction but not acquisition or expression of morphine-induced CPA in rats. The blockade of CPA extinction induced by SSZ was abolished by sodium butyrate, an inhibitor of histone deacetylase. Thus, the IKK/NF-κB signaling pathway might play a critical role in the extinction of morphine-induced CPA in rats and might be a potential pharmacotherapy target for opiate addiction.
抑制剂 κB 蛋白激酶/核因子 κB（IKK/NF-κB）信号通路对于突触可塑性至关重要。然而，IKK/NF-κB 在药物戒断相关条件性位置厌恶（CPA）记忆中的作用尚不清楚。在这里，我们表明，通过柳氮磺胺吡啶（SSZ；10mM，脑室内）抑制 IKK/NF-κB 选择性地阻断了吗啡诱导的 CPA 在大鼠中的消退，但不影响获得或表达。SSZ 诱导的 CPA 消退阻断被组蛋白去乙酰化酶抑制剂丁酸钠所消除。因此，IKK/NF-κB 信号通路可能在吗啡诱导的 CPA 在大鼠中的消退中发挥关键作用，并且可能是阿片类药物成瘾的潜在药物治疗靶点。
