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GABAergic neurons in the insular cortex play an important rol
AAV-hM3D(Gq) and AAV-hM4D(Gi) were used for chemogenetics manipulation. (From BrainVTA)
The viruses used from BrainVTA in this article are in the table below
Chemogenetics  PT-0489 rAAV-VGAT1-hM3D(Gq)-mCherry-WPRE-pA
 PT-0488 rAAV-VGAT1-hM4D(Gi)-mCherry-WPRE-pA
Control  PT-0325 rAAV-VGAT1-mCherry-WPRE-Pa
Kuisheng Sun, Lifei Xiao, Yiyang Wu, Di Zuo, Chun Zhang, Shenhai Liu, Zhenquan He, Shikuo Rong, Feng Wang, Tao Sun
Pub Date: 2020-04-08, DOI: 10.1016/j.lfs.2020.117655, Email:
AIMS There have been recent reports that reconsolidation-based interventions attenuate drug reward memories in rodents. The insular cortex (IC) is an essential part of neural circuits that underlie cue-drug memory reconsolidation. GABAergic interneurons in the IC are a potent control on network excitability and play an important role in the inhibitory mediation of reward circuits. However, the function of GABAergic neurons in the IC for memory reconsolidation remains unclear; therefore, we conducted this study to clarify this. MAIN METHODS We applied morphine-induced conditioned place preference (mCPP) paradigm and pharmacogenetic techniques to study the mediation effect of GABAergic neurons in the IC on mCPP reconsolidation. Moreover, we preliminarily explored the possible mechanisms of mediating GABAergic neurons in the IC involved in mCPP reconsolidation by assessing Arc and Erg-1 protein levels in the IC. KEY FINDINGS We found that post-retrieval immediate activation of GABAergic neurons in the IC impaired mCPP reconsolidation. In addition, this effect was not reversed by a priming morphine injection. Further, post-retrieval inhibition and non-retrieval excitation of GABAergic neurons in the IC had no effect on mCPP. SIGNIFICANCE Taken together, our findings suggest that GABAergic neurons in the IC are closely involved in mCPP reconsolidation. Specifically, their excitation could eliminate established mCPP and prevent the relapse risk by disruption of the reconsolidation. The underlying molecular biological mechanisms could involve reduced Arc and Erg-1 levels.

Figure 1. Schematic diagram of the experimental protocol.
This study is aimed to explore the relationship between GABAergic neurons in the IC and the reconsolidation of morphine reward memory. The authors employ morphine-induced conditioned place preference (mCPP) as a behavioural paradigm and examine whether the mediation of GABAergic neurons in the IC of morphine-addicted rats via pharmacogenetics technology affects reward memory reconsolidation. These results revealed that the mediating GABAergic neurons in the IC could be a potential method to prevent drug craving and relapse.
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