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Hydrogen Sulfide Reverses Aging-Associated Amygdalar Synaptic Plasticity and Fear Memory Deficits in Rats

Overview of attention for article published in Frontiers in Neuroscience, June 2018
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Title
Hydrogen Sulfide Reverses Aging-Associated Amygdalar Synaptic Plasticity and Fear Memory Deficits in Rats
Published in
Frontiers in Neuroscience, June 2018
DOI 10.3389/fnins.2018.00390
Pubmed ID
Authors

Jin-Qiong Zhan, Li-Li Zheng, Hai-Bo Chen, Bin Yu, Wei Wang, Ting Wang, Bo Ruan, Bin-Xing Pan, Juan-Ru Chen, Xue-Fen Li, Bo Wei, Yuan-Jian Yang

Abstract

As an endogenous neuromodulator, hydrogen sulfide (H2S) exerts multiple biological effects in the brain. Previous studies have shown that H2S is involved in the regulation of neural synaptic plasticity and cognition in healthy rodents. It is well known that there is a progressive decline of cognitive function that occurs with increased age. The purpose of this study was to investigate the role of H2S in aging-associated amygdalar synaptic plasticity and cued fear memory deficits as well as to explore the underlying mechanisms. We found that H2S levels in the amygdala were significantly lower in aged rats when compared with healthy adult rates, which displayed significant deficits in long-term potentiation (LTP) in the thalamo-lateral amygdala (LA) pathway and amygdala-dependent cued fear memory. Bath application of an H2S donor, sodium hydrogen sulfide (NaHS), significantly reversed the impaired LTP in brain slices from aged rats, and intra-LA infusion of NaHS restored the cued fear memory in aged rats. Mechanismly, we found that H2S treatment significantly enhanced NMDAR-mediated synaptic responses in the thalamo-LA pathway of aged rats. Notably, GluN2B-containing NMDARs, but not GluN2A-containing NMDARs, contributed to the effects of H2S on aging-associated impairments of amygdalar LTP and fear memory, because applying GluN2B antagonist could abolish the beneficial effects of NaHS treatment on amygdalar LTP and cognitive performance in aged rats. Collectively, these results show that H2S can reverse aging-associated amygdalar synaptic plasticity and fear memory deficits by restoring the function of GluN2B-containing NMDARs, suggesting that supplement of H2S might be a therapeutic approach for aging-related cognitive disorders.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 22 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 22 100%

Demographic breakdown

Readers by professional status Count As %
Student > Master 4 18%
Student > Bachelor 3 14%
Student > Ph. D. Student 3 14%
Student > Doctoral Student 1 5%
Professor 1 5%
Other 2 9%
Unknown 8 36%
Readers by discipline Count As %
Neuroscience 5 23%
Medicine and Dentistry 3 14%
Agricultural and Biological Sciences 2 9%
Economics, Econometrics and Finance 1 5%
Pharmacology, Toxicology and Pharmaceutical Science 1 5%
Other 2 9%
Unknown 8 36%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 23 October 2018.
All research outputs
#17,716,345
of 25,967,142 outputs
Outputs from Frontiers in Neuroscience
#8,262
of 11,739 outputs
Outputs of similar age
#223,650
of 344,552 outputs
Outputs of similar age from Frontiers in Neuroscience
#184
of 233 outputs
Altmetric has tracked 25,967,142 research outputs across all sources so far. This one is in the 21st percentile – i.e., 21% of other outputs scored the same or lower than it.
So far Altmetric has tracked 11,739 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 11.1. This one is in the 24th percentile – i.e., 24% of its peers scored the same or lower than it.
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