Evidence map›Paper›PMID 36917193›Full record

ArticleThe Journal of clinical investigation2023

Elevated prelimbic cortex-to-basolateral amygdala circuit activity mediates comorbid anxiety-like behaviors associated with chronic pain.

Feng Gao, Jie Huang, Guo-Bin Huang, Qiang-Long You, Shan Yao, Shen-Ting Zhao, Jian Liu, Cui-Hong Wu, Gui-Fu Chen, Shi-Min Liu and 6 more

Open access · goldAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
10.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

43 citing papers in PubMed, 58 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 1 country.

Feng GaoDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Jie HuangDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Guo-Bin HuangDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Qiang-Long YouDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Shan YaoDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Shen-Ting ZhaoDepartment of Physiology, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Jian LiuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Cui-Hong WuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Gui-Fu ChenDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Shi-Min LiuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Zongyan YuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Yan-Ling ZhouDepartment of Psychiatry, Affiliated Brain Hospital of Guangzhou Medical University, Guangzhou, China.
Yu-Ping NingDepartment of Psychiatry, Affiliated Brain Hospital of Guangzhou Medical University, Guangzhou, China.
Shenquan LiuSchool of Mathematics, South China University of Technology, Guangzhou, China.
Bing-Jie HuDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Xiang-Dong SunDepartment of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, and Emergency Department of the Second Affiliated Hospital, School of Basic Medicine, Guangzhou Medical University, Guangzhou, China.
Second Affiliated Hospital of Guangzhou Medical University · CNGuangzhou Medical University · CNGuangdong Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pain can cause both hyperalgesia and anxiety symptoms. However, how the two components are encoded in the brain remains unclear. The prelimbic cortex (PrL), a critical brain region for both nociceptive and emotional modulations, serves as an ideal medium for comparing how the two components are encoded. We report that PrL neurons projecting to the basolateral amygdala (PrLBLA) and those projecting to the ventrolateral periaqueductal gray (PrLl/vlPAG) were segregated and displayed elevated and reduced neuronal activity, respectively, during pain chronicity. Consistently, optogenetic suppression of the PrL-BLA circuit reversed anxiety-like behaviors, whereas activation of the PrL-l/vlPAG circuit attenuated hyperalgesia in mice with chronic pain. Moreover, mechanistic studies indicated that elevated TNF-α/TNFR1 signaling in the PrL caused increased insertion of GluA1 receptors into PrLBLA neurons and contributed to anxiety-like behaviors in mice with chronic pain. Together, these results provide insights into the circuit and molecular mechanisms in the PrL for controlling pain-related hyperalgesia and anxiety-like behaviors.

Indexed as

Basolateral Nuclear ComplexChronic PainAnimalsAnxietyCerebral CortexHyperalgesiaMiceBehaviorCytokinesNeurosciencePain

Identifiers

PMID36917193
PMCPMC10145931
OpenAlexW4324128937

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.