2017年3月7日， 國際期刊《Frontiers in Behavioral Neuroscience》線上發表了中國科學院心理研究所隋南研究組的一篇研究論文， 論文揭示成癮戒斷記憶再鞏固的DNA甲基化調控機制。
成癮戒斷引起的負性情緒記憶長期存在， 是導致成癮者複吸的關鍵因素。 再鞏固是長時記憶加工的重要階段， 為破壞長時程病理性記憶提供了干預的“視窗”。 但成癮階段記憶再鞏固的核團及其轉錄調控機制尚不清楚。
研究組採用嗎啡-納洛酮誘導的條件位置厭惡(CPA)範式， 通過核團定位注射DNA甲基化抑制劑5-aza的方法探討了這一問題。 大鼠經過CPA訓練後形成了嗎啡戒斷相關的負性情緒記憶，
該研究首次發現DNA甲基化在成癮戒斷記憶再鞏固中發揮重要作用， 此外， 該研究還發現島葉AI和杏仁核BLA亞區在負性情緒記憶再鞏固中可能發揮不同的調控作用。 這為探索干預成癮記憶的新靶點提供了新證據， 未來有必要針對DNA甲基化調控成癮記憶的內在分子機制做進一步探究。
原文連結：
Distinctive Roles of 5-aza-2′-deoxycytidine in Anterior Agranular Insular and Basolateral Amygdala in Reconsolidation of Aversive memory Associated with Morphine in Rats
原文摘要：
5-aza-2′-deoxycytidine (5-aza), an inhibitor of DNA methyltransferases (DNMTs), has been implicated in aversive memory and the functionof brain region involved in processing emotion. However, little is known about the role of 5-aza in the reconsolidation of opiate withdrawal memory. In the present study, using the morphine-naloxone induced conditioned place aversion (CPA) model in rats, we injected 5-aza into agranular insular (AI), granular insular (GI), basolateral amygdala (BLA) and central amygdala (CeA) immediately after the memory retrieval and tested the behavioral consequences at 24 h, 7 and 14 days after retrieval test. We found that 5-aza injection into AI disrupted the reconsolidation of morphine-associated withdrawal memory, but 5-aza injection into GI had no impact on the reconsolidation. Meanwhile, 5-aza injection into BLA but not CeA attenuated the withdrawal memory trace 14 days later. However, 5-aza administration to rats, in the absence of memory reactivation, had no effect on morphine-associated withdrawal memory. These findings suggest that 5-aza interferes with the reconsolidation of opiate withdrawal memory, and the roles of insular and amygdala in reconsolidation are distinctive.
作者：隋南 點擊：次