↓ Skip to main content

Sensitization of neurons in the central nucleus of the amygdala via the decreased GABAergic inhibition contributes to the development of neuropathic pain-related anxiety-like behaviors in rats

Overview of attention for article published in Molecular Brain, October 2014
Altmetric Badge

Mentioned by

twitter
1 tweeter

Citations

dimensions_citation
34 Dimensions

Readers on

mendeley
70 Mendeley
Title
Sensitization of neurons in the central nucleus of the amygdala via the decreased GABAergic inhibition contributes to the development of neuropathic pain-related anxiety-like behaviors in rats
Published in
Molecular Brain, October 2014
DOI 10.1186/s13041-014-0072-z
Pubmed ID
Authors

Hong Jiang, Dong Fang, Ling-Yu Kong, Zi-Run Jin, Jie Cai, Xue-Jing Kang, You Wan, Guo-Gang Xing

Abstract

BackgroundDespite high prevalence of anxiety accompanying with chronic pain, the mechanisms underlying pain-related anxiety are largely unknown. With its well-documented role in pain and emotion processing, the amygdala may act as a key player in pathogenesis of neuropathic pain-related anxiety. Pain-related plasticity and sensitization of CeA (central nucleus of the amygdala) neurons have been shown in several models of chronic pain. In addition, firing pattern of neurons with spike output can powerfully affect functional output of the brain nucleus, and GABAergic neurons are crucial in the modulation of neuronal excitability. In this study, we first investigated whether pain-related plasticity (e.g. alteration of neuronal firing patterns) and sensitization of CeA neurons contribute to nerve injury-evoked anxiety in neuropathic rats. Furthermore, we explored whether GABAergic disinhibition is responsible for regulating firing patterns and intrinsic excitabilities of CeA neurons as well as for pain-related anxiety in neuropathic rats.ResultsWe discovered that spinal nerve ligation (SNL) produced neuropathic pain-related anxiety-like behaviors in rats, which could be specifically inhibited by intra-CeA administration of anti-anxiety drug diazepam. Moreover, we found potentiated plasticity and sensitization of CeA neurons in SNL-induced anxiety rats, of which including: 1) increased burst firing pattern and early-adapting firing pattern; 2) increased spike frequency and intrinsic excitability; 3) increased amplitude of both after-depolarized-potential (ADP) and sub-threshold membrane potential oscillation. In addition, we observed a remarkable reduction of GABAergic inhibition in CeA neurons in SNL-induced anxiety rats, which was proved to be important for altered firing patterns and hyperexcitability of CeA neurons, thereby greatly contributing to the development of neuropathic pain-related anxiety. Accordantly, activation of GABAergic inhibition by intra-CeA administration of muscimol, a selective GABAA receptors agonist, could inhibit SNL-induced anxiety-like behaviors in neuropathic rats. By contrast, suppression of GABAergic inhibition by intra-CeA administration of bicuculline, a selective GABAA receptors antagonist, produced anxiety-like behavior in normal rats.ConclusionsThis study suggests that reduction of GABAergic inhibition may be responsible for potentiated plasticity and sensitization of CeA neurons, which likely underlie the enhanced output of amygdala and neuropathic pain-related anxiety in SNL rats.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 70 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
France 1 1%
Unknown 69 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 22 31%
Researcher 13 19%
Student > Master 11 16%
Student > Bachelor 7 10%
Student > Doctoral Student 5 7%
Other 6 9%
Unknown 6 9%
Readers by discipline Count As %
Neuroscience 20 29%
Agricultural and Biological Sciences 16 23%
Medicine and Dentistry 12 17%
Psychology 5 7%
Pharmacology, Toxicology and Pharmaceutical Science 4 6%
Other 3 4%
Unknown 10 14%

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 05 October 2014.
All research outputs
#6,627,488
of 8,702,492 outputs
Outputs from Molecular Brain
#360
of 459 outputs
Outputs of similar age
#130,689
of 197,595 outputs
Outputs of similar age from Molecular Brain
#22
of 25 outputs
Altmetric has tracked 8,702,492 research outputs across all sources so far. This one is in the 13th percentile – i.e., 13% of other outputs scored the same or lower than it.
So far Altmetric has tracked 459 research outputs from this source. They receive a mean Attention Score of 4.1. This one is in the 3rd percentile – i.e., 3% of its peers scored the same or lower than it.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 197,595 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 19th percentile – i.e., 19% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 25 others from the same source and published within six weeks on either side of this one. This one is in the 4th percentile – i.e., 4% of its contemporaries scored the same or lower than it.