scholarly journals Ontogeny of contextual fear memory formation, specificity, and persistence in mice

2012 ◽  
Vol 19 (12) ◽  
pp. 598-604 ◽  
Author(s):  
K. G. Akers ◽  
M. Arruda-Carvalho ◽  
S. A. Josselyn ◽  
P. W. Frankland
2015 ◽  
Vol 41 (7) ◽  
pp. 1849-1864 ◽  
Author(s):  
Ying Han ◽  
Yixiao Luo ◽  
Jia Sun ◽  
Zengbo Ding ◽  
Jianfeng Liu ◽  
...  

2021 ◽  
Vol 28 (8) ◽  
pp. 248-253
Author(s):  
Kiley Martin ◽  
Madeline Musaus ◽  
Shaghayegh Navabpour ◽  
Aspen Gustin ◽  
W. Keith Ray ◽  
...  

Neuroreport ◽  
2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Cui Zhao ◽  
Bo Zhou ◽  
Junjie Cao ◽  
Yafang Zhang ◽  
Wei Li ◽  
...  

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Min Soo Kang ◽  
Jin-Hee Han

AbstractFormation of temporal association memory and context-specific fear memory is thought to require medial entorhinal cortex (MEC) inputs to the hippocampus during learning events. However, whether the MEC inputs are also involved in memory formation during a post-learning period has not been directly tested yet. To examine this possibility, we optogenetically inhibited axons and terminals originating from bilateral dorsal MEC excitatory neurons in the dorsal hippocampus for 5 min right after contextual fear conditioning (CFC). Mice expressing eNpHR3.0 exhibited significantly less freezing compared to control mice expressing EGFP alone during retrieval test in the conditioned context 1 day after learning. In contrast, the same optogenetic inhibition of MEC inputs performed 30 min before retrieval test did not affect freezing during retrieval test, excluding the possibility of non-specific deleterious effect of optical inhibition on retrieval process. These results support that contextual fear memory formation requires MEC inputs to the hippocampus during a post-learning period.


2006 ◽  
Vol 26 (23) ◽  
pp. 9094-9104 ◽  
Author(s):  
Keiko Mizuno ◽  
Laurence Ris ◽  
Amelia Sánchez-Capelo ◽  
Emile Godaux ◽  
K. Peter Giese

ABSTRACT In neurons, the Ca2+/calmodulin (CaM) kinase cascade transduces Ca2+ signaling into gene transcription. The CaM kinase cascade is known to be important for brain development as well as memory formation in adult brain, although the functions of some cascade members remain unknown. Here we have generated null and hypomorphic mutants to study the physiological role of CaM kinase kinase α (CaMKKα), which phosphorylates and activates both CaM kinase I (CaMKI) and CaMKIV, the output kinases of the cascade. We show that CaMKKα is dispensable for brain development and long-term potentiation in adult hippocampal CA1 synapses. We find that CaMKKα is required for hippocampus-dependent contextual fear memory, but not spatial memory, formation. Surprisingly, CaMKKα is important for contextual fear memory formation in males but not in females. We show that in male mice, contextual fear conditioning induces up-regulation of hippocampal mRNA expression of brain-derived neurotrophic factor (BDNF) in a way that requires CaMKKα, while in female mice, contextual fear conditioning induces down-regulation of hippocampal BDNF mRNA expression that does not require CaMKKα. Additionally, we demonstrate sex-independent up-regulation in hippocampal nerve growth factor-inducible gene B mRNA expression that does not require CaMKKα. Thus, we show that CaMKKα has a specific complex role in memory formation in males.


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