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Dorsal Hippocampus to Infralimbic Cortex Circuit is Essential
A cocktail of tTA and TRE-CRE viruses were used to conditionally delete ERK2 in the IL. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Control  PT-0241 rAAV2/R-hSyn-EGFP-WPRE-pA
Activity-dependent  PT-0554 rAAV2/9-TRE-CRE-2a-EYFP-WPRE-pA
 PT-0140 rAAV2/9-TRE-EYFP-WPRE-pA
 PT-0553 rAAV2/9-EF1a-tTA-WPRE-pA
Cheng Qin, Xin-Lan Bian, Hai-Yin Wu, Jia-Yun Xian, Cheng-Yun Cai,Yu-Hui Lin, Ying Zhou, Xiao-Lin Kou, Lei Chang, Chun-Xia Luo and Dong-Ya Zhu
Pub Date: 2020-11-14, DOI: 10.1093/cercor/bhaa320, Email: [email protected]
Posttraumatic stress disorder subjects usually show impaired recall of extinction memory, leading to extinguished fear relapses. However, little is known about the neural mechanisms underlying the impaired recall of extinction memory. We show here that the activity of dorsal hippocampus (dHPC) to infralimbic (IL) cortex circuit is essential for the recall of fear extinction memory in male mice. There were functional neural projections from the dHPC to IL. Using optogenetic manipulations, we observed that silencing the activity of dHPC-IL circuit inhibited recall of extinction memory while stimulating the activity of dHPC-IL circuit facilitated recall of extinction memory. “Impairment of extinction consolidation caused by” conditional deletion of extracellular signal-regulated kinase 2 (ERK2) in the IL prevented the dHPC-IL circuit-mediated recall of extinction memory. Moreover, silencing the dHPC-IL circuit abolished the effect of intra-IL microinjection of ERK enhancer on the recall of extinction memory. Together, we identify a dHPC to IL circuit that mediates the recall of extinction memory, and our data suggest that the dysfunction of dHPC-IL circuit and/or impaired extinction consolidation may contribute to extinguished fear relapses.
In this study, the authors want to explore the neural mechanisms underlying the impaired recall of extinction memory. The findings show that the dHPC to IL circuit is essential for the recall of extinction memory.
 
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