scholarly journals Bidirectional Effects of Cannabidiol on Contextual Fear Memory Extinction

2016 ◽  
Vol 7 ◽  
Author(s):  
Chenchen Song ◽  
Carl W. Stevenson ◽  
Francisco S. Guimaraes ◽  
Jonathan L. C. Lee
Keyword(s):  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Memory Extinction ◽  
Bidirectional Effects

scholarly journals Glycyrrhizin Treatment Facilitates Extinction of Conditioned Fear Responses After a Single Prolonged Stress Exposure in Rats

2018 ◽  
Vol 45 (6) ◽  
pp. 2529-2539 ◽  
Author(s):  
Shuhua Lai ◽  
Gangwei Wu ◽  
Zhixian Jiang
Keyword(s):  
Critical Role ◽  
Fear Memory ◽  
Fear Extinction ◽  
Chromosomal Protein ◽  
Single Prolonged Stress ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Memory Extinction ◽  
Prolonged Stress ◽  
Tlr4 Antagonist

Background/Aims: Impaired fear memory extinction is widely considered a key mechanism of post-traumatic stress disorder (PTSD). Recent studies have suggested that neuroinflammation after a single prolonged stress (SPS) exposure may play a critical role in the impaired fear memory extinction. Studies have shown that high mobility group box chromosomal protein 1 (HMGB-1) is critically involved in neuroinflammation. However, the role of HMGB-1 underlying the development of impairment of fear memory extinction is still not known. Methods: Thus, we examined the levels of HMGB-1 in the basolateral amygdala (BLA) following SPS using Western blot and evaluated the levels of microglia and astrocytes activation in the BLA after SPS using immunohistochemical staining. We then examined the effects of pre-SPS intra-BLA administration of glycyrrhizin, an HMGB1 inhibitor, or LPS-RS, a competitive TLR4 antagonist, on subsequent post-SPS fear extinction. Results: We found that SPS treatment prolonged the extinction of contextual fear memory after the SPS. The impairment of SPS-induced extinction of contextual fear memory was associated with increased HMGB1 and Toll-like receptor 4 (TLR4) levels in the BLA. Additionally, the impairment of SPS-induced extinction of contextual fear memory was associated with increased activation of microglia and astrocyte in the BLA. Intra-BLA administrations of glycyrrhizin (HMGB-1 inhibitor) or LPS-RS (TLR4 antagonist) can prevent the development of SPS-induced fear extinction impairment. Conclusion: Taken together, these results suggested that SPS treatment may not only produce short term effects on the HMGB1/TLR4-mediated pro-inflammation, but alter the response of microglia and astrocytes to the exposure to fear associated contextual stimuli.

scholarly journals Torpor enhances synaptic strength and restores memory performance in a mouse model of Alzheimer’s disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Christina F. de Veij Mestdagh ◽  
Jaap A. Timmerman ◽  
Frank Koopmans ◽  
Iryna Paliukhovich ◽  
Suzanne S. M. Miedema ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Mouse Model ◽  
Memory Performance ◽  
Long Term Potentiation ◽  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Model Of Alzheimer’S Disease ◽  
Term Potentiation

AbstractHibernation induces neurodegeneration-like changes in the brain, which are completely reversed upon arousal. Hibernation-induced plasticity may therefore be of great relevance for the treatment of neurodegenerative diseases, but remains largely unexplored. Here we show that a single torpor and arousal sequence in mice does not induce dendrite retraction and synapse loss as observed in seasonal hibernators. Instead, it increases hippocampal long-term potentiation and contextual fear memory. This is accompanied by increased levels of key postsynaptic proteins and mitochondrial complex I and IV proteins, indicating mitochondrial reactivation and enhanced synaptic plasticity upon arousal. Interestingly, a single torpor and arousal sequence was also sufficient to restore contextual fear memory in an APP/PS1 mouse model of Alzheimer’s disease. Our study demonstrates that torpor in mice evokes an exceptional state of hippocampal plasticity and that naturally occurring plasticity mechanisms during torpor provide an opportunity to identify unique druggable targets for the treatment of cognitive impairment.

PKMζ maintains remote contextual fear memory by inhibiting GluA2-dependent AMPA receptor endocytosis in the prelimbic cortex

Neuroscience ◽  
2021 ◽  
Author(s):  
Lucas A. Marcondes ◽  
Jociane de C. Myskiw ◽  
Eduarda G. Nachtigall ◽  
Rodrigo F. Narvaes ◽  
Ivan Izquierdo ◽  
...  
Keyword(s):  
Ampa Receptor ◽  
Fear Memory ◽  
Prelimbic Cortex ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Receptor Endocytosis

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 ◽  
...  
Keyword(s):  
Fear Memory ◽  
Contextual Fear ◽  
Contextual Fear Memory ◽  
Hippocampal Ca1
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