scholarly journals Visually cued fear conditioning test for memory impairment related to cortical function

2020 ◽  
Vol 40 (4) ◽  
pp. 371-375
Author(s):  
Kazuya Kuboyama ◽  
Yuki Shirakawa ◽  
Koji Kawada ◽  
Naoki Fujii ◽  
Daiki Ojima ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Memory Impairment ◽  
Cortical Function ◽  
Fear Conditioning Test

Targeted invalidation of CCK2 receptor gene induces anxiolytic-like action in light–dark exploration, but not in fear conditioning test

2005 ◽  
Vol 181 (2) ◽  
pp. 347-357 ◽  
Author(s):  
Sirli Raud ◽  
Jürgen Innos ◽  
Urho Abramov ◽  
Ain Reimets ◽  
Sulev Kõks ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Receptor Gene ◽  
Cck2 Receptor ◽  
Fear Conditioning Test

scholarly journals Contextual and Cued Fear Conditioning Test Using a Video Analyzing System in Mice

10.3791/50871 ◽  
2014 ◽  
Author(s):  
Hirotaka Shoji ◽  
Keizo Takao ◽  
Satoko Hattori ◽  
Tsuyoshi Miyakawa
Keyword(s):  
Fear Conditioning ◽  
Fear Conditioning Test

Fear conditioning to discontinuous auditory cues requires perirhinal cortical function.

2008 ◽  
Vol 122 (5) ◽  
pp. 1178-1185 ◽  
Author(s):  
D. B. Kholodar-Smith ◽  
T. A. Allen ◽  
T. H. Brown
Keyword(s):  
Fear Conditioning ◽  
Cortical Function ◽  
Auditory Cues

scholarly journals piRNAs in the Olfactory Bulb Related to Fear Conditioning can Migrate from the Brain to the Germline

2021 ◽  
Vol 3 (5) ◽  
pp. 132-136
Author(s):  
Sicong Chen
Keyword(s):  
Olfactory Bulb ◽  
Fear Conditioning ◽  
Small Rnas ◽  
Memory Formation ◽  
Virus Vector ◽  
Single Nucleotide ◽  
The Brain ◽  
Fear Conditioning Test

Small RNAs have been shown to be crucial in the mechanisms of transgenerational memory. Precisely, piRNAs have previously been thought to only exist in the germline and are related to transgenerational memory. To determine if the offspring inherits memory due to piRNA transmission, we conducted odor fear-conditioning tests and identified a piRNA that increased in abundance. That piRNA is thought to be involved in memory formation of the fear-conditioning test. We then used a virus vector to manipulate a single nucleotide of that piRNA sequence to see if it can migrate from the olfactory bulb to the germline. The data should theoretically indicate whether the mutant piRNA has migrated from the olfactory bulb to the germline of the mice.

scholarly journals Elamipretide (SS-31) improves mitochondrial dysfunction, synaptic and memory impairment induced by lipopolysaccharide in mice

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Weixing Zhao ◽  
Zhipeng Xu ◽  
Jiangbei Cao ◽  
Qiang Fu ◽  
Yishuang Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Learning And Memory ◽  
Dendritic Spines ◽  
Memory Impairment ◽  
Memory Performance ◽  
Contextual Fear Conditioning ◽  
Contextual Fear ◽  
And Oxidative Stress ◽  
Fear Conditioning Test

Abstract Background It is widely accepted that mitochondria have a direct impact on neuronal function and survival. Oxidative stress caused by mitochondrial abnormalities play an important role in the pathophysiology of lipopolysaccharide (LPS)-induced memory impairment. Elamipretide (SS-31) is a novel mitochondrion-targeted antioxidant. However, the impact of elamipretide on the cognitive sequelae of inflammatory and oxidative stress is unknown. Methods We utilized MWM and contextual fear conditioning test to assess hippocampus-related learning and memory performance. Molecular biology techniques and ELISA were used to examine mitochondrial function, oxidative stress, and the inflammatory response. TUNEL and Golgi-staining was used to detect neural cell apoptosis and the density of dendritic spines in the mouse hippocampus. Results Mice treated with LPS exhibited mitochondrial dysfunction, oxidative stress, an inflammatory response, neural cell apoptosis, and loss of dendritic spines in the hippocampus, leading to impaired hippocampus-related learning and memory performance in the MWM and contextual fear conditioning test. Treatment with elamipretide significantly ameliorated LPS-induced learning and memory impairment during behavioral tests. Notably, elamipretide not only provided protective effects against mitochondrial dysfunction and oxidative stress but also facilitated the regulation of brain-derived neurotrophic factor (BDNF) signaling, including the reversal of important synaptic-signaling proteins and increased synaptic structural complexity. Conclusion These findings indicate that LPS-induced memory impairment can be attenuated by the mitochondrion-targeted antioxidant elamipretide. Consequently, elamipretide may have a therapeutic potential in preventing damage from the oxidative stress and neuroinflammation that contribute to perioperative neurocognitive disorders (PND), which makes mitochondria a potential target for treatment strategies for PND.

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