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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
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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.

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The data shown below were compiled from readership statistics for 94 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
France 1 1%
Unknown 93 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 27 29%
Researcher 15 16%
Student > Master 12 13%
Student > Bachelor 7 7%
Student > Doctoral Student 5 5%
Other 12 13%
Unknown 16 17%
Readers by discipline Count As %
Neuroscience 29 31%
Agricultural and Biological Sciences 17 18%
Medicine and Dentistry 14 15%
Pharmacology, Toxicology and Pharmaceutical Science 7 7%
Psychology 4 4%
Other 4 4%
Unknown 19 20%
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 05 October 2014.
All research outputs
#18,379,655
of 22,765,347 outputs
Outputs from Molecular Brain
#858
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Outputs of similar age
#181,470
of 254,034 outputs
Outputs of similar age from Molecular Brain
#22
of 25 outputs
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