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Regulation of Cued Fear Expression via Corticotropin-Releasin
AAV- hM3D(Gq) was used for chemogenetics manipulation. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Chemogenetics  PT-0042 AAV-EF1a-DIO-hM3D(Gq)-mCherry
Control  PT-0013 AAV-EF1a-DIO-mCherry
 PT-0012 AAV-EF1a-DIO-EYFP
Yin Lv, Peng Chen, Qing-Hong Shan, Xin-Ya Qin, Xiu-Hong Qi, Jiang-Ning Zhou
Pub Date: 2020-10-14, DOI: 10.1007/s12264-020-00592-6, Email: [email protected]
The ventral part of the anteromedial thalamic nucleus (AMv) is in a position to convey information to the cortico-hippocampal-amygdalar circuit involved in the processing of fear memory. Corticotropin-releasing-factor (CRF) neurons are closely associated with the regulation of stress and fear. However, few studies have focused on the role of thalamic CRF neurons in fear memory. In the present study, using a conditioned fear paradigm in CRF transgenic mice, we found that the c-Fos protein in the AMv CRF neurons was significantly increased after cued fear expression. Chemogenetic activation of AMv CRF neurons enhanced cued fear expression, whereas inhibition had the opposite effect on the cued fear response. Moreover, chemogenetic manipulation of AMv CRF neurons did not affect fear acquisition or contextual fear expression. In addition, anterograde tracing of projections revealed that AMv CRF neurons project to wide areas of the cerebral cortex and the limbic system. These results uncover a critical role of AMv CRF neurons in the regulation of conditioned fear memory.

Figure 1. AMv CRF neurons project to wide areas of the cerebral cortex and limbic system.
This study is aimed to explore the role of thalamic CRF neurons in fear memory. Using a classical fear conditioning paradigm and chemogenetic manipulation, the authors uncover a critical role of AMv CRF neurons in the regulation of conditioned fear memory.
 
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