scholarly journals Overexpression of SIRT6 in the hippocampal CA1 impairs the formation of long-term contextual fear memory

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Xi Yin ◽  
Yuan Gao ◽  
Hai-Shui Shi ◽  
Li Song ◽  
Jie-Chao Wang ◽  
...  
Author(s):  
Ye-Fei Chen ◽  
Zi-Xiang Chen ◽  
Run-Hua Wang ◽  
Yan-Wei Shi ◽  
Li Xue ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Smitha Karunakaran

AbstractIn this study we demonstrate that 2 month old APPswe/PS1dE9 mice, a transgenic model of Alzheimer’s disease, exhibited intact short-term memory in Pavlovian hippocampal—dependent contextual fear learning task. However, their long-term memory was impaired. Intra-CA1 infusion of isoproterenol hydrochloride, the β-adrenoceptor agonist, to the ventral hippocampus of APPswe/PS1dE9 mice immediately before fear conditioning restored long-term contextual fear memory. Infusion of the β-adrenoceptor agonist + 2.5 h after fear conditioning only partially rescued the fear memory, whereas infusion at + 12 h post conditioning did not interfere with long-term memory persistence in this mouse model. Furthermore, Intra-CA1 infusion of propranolol, the β-adrenoceptor antagonist, administered immediately before conditioning to their wildtype counterpart impaired long-term fear memory, while it was ineffective when administered + 4 h and + 12 h post conditioning. Our results indicate that, long-term fear memory persistence is determined by a unique β-adrenoceptor sensitive time window between 0 and + 2.5 h upon learning acquisition, in the ventral hippocampal CA1 of APPswe/PS1dE9 mice. On the contrary, β-adrenoceptor agonist delivery to ventral hippocampal CA1 per se did not enhance innate anxiety behaviour in open field test. Thus we conclude that, activation of learning dependent early β-adrenoceptor modulation underlies and is necessary to promote long-term fear memory persistence in APPswe/PS1dE9.


IBRO Reports ◽  
2019 ◽  
Vol 6 ◽  
pp. S185-S186
Author(s):  
Zhengdong Lin ◽  
Si Chen ◽  
Kai-Leng Tan ◽  
Wen Tan

2012 ◽  
Vol 72 (3) ◽  
pp. 182-190 ◽  
Author(s):  
Hanoch Kaphzan ◽  
Pepe Hernandez ◽  
Joo In Jung ◽  
Kiriana K. Cowansage ◽  
Katrin Deinhardt ◽  
...  

PLoS ONE ◽  
2016 ◽  
Vol 11 (5) ◽  
pp. e0153102 ◽  
Author(s):  
Birger Scholz ◽  
Amie N. Doidge ◽  
Philip Barnes ◽  
Jeremy Hall ◽  
Lawrence S. Wilkinson ◽  
...  

2009 ◽  
Vol 24 (S1) ◽  
pp. 1-1
Author(s):  
S. Kida

Activity-dependent gene expression through activation of Ca2+-CREB signal transduction pathways has been thought to play a central role in fear memory formation. On the other hand, retrieval of fear memory triggers two time-dependent phases of reactivated memory; reconsolidation and extinction. To understand the mechanisms for determining the fate of the reactivated fear memory, we investigated roles of CREB in reconsolidation and extinction of contextual fear memory and then analyzed the brain-regions regulating reconsolidation and extinction by identifying regions where CREB-mediated gene expression is activated and then examining the role of protein synthesis in those regions on reconsolidation and extinction. We first showed that activation of CREB-mediated transcription is required for reconsolidation and long-term extinction of contextual fear memory. Using immunocytochemical analyses, we demonstrated that CREB is activated in the hippocampus/amygdala and amygdala/medial prefrontal cortex (mPFC) in the reconsolidation and extinction phases, respectively. Similar results were observed by analyzing the expression of a CREB-dependent gene, Arc. We finally showed that reconsolidation and long-term extinction of the contextual fear memory depended on new gene expression in the hippocampus/amygdala and amygdala/mPFC, respectively. Thus reactivated contextual fear memory is reconsolidated or extinguished through distinct CREB-mediated gene expression regulation in the hippocampus, amygdala and mPFC.


Sign in / Sign up

Export Citation Format

Share Document