Evidence map›Paper›PMID 27364923›Full record

ArticleScientific reports2016

TRPV1-mediated presynaptic transmission in basolateral amygdala contributes to visceral hypersensitivity in adult rats with neonatal maternal deprivation.

Ying Xiao, Xiaoqi Chen, Ping-An Zhang, Qiya Xu, Hang Zheng, Guang-Yin Xu

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. Neural circuits regulating visceral pain.Communications biology · 2024
    Review
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  6. Identification of a Glutamatergic Claustrum-Anterior Cingulate Cortex Circuit for Visceral Pain Processing.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Article
  8. Supraspinal Mechanisms of Intestinal Hypersensitivity.Cellular and molecular neurobiology · 2022
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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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

6 authors at 1 institution in 1 country.

Ying XiaoJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Laboratory of Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou 215123, P.R. China.
Xiaoqi ChenDepartment of Gastroenterology, the First Affiliated Hospital of Henan College of Traditional Chinese Medicine, Zhengzhou 45000, P.R. China.
Ping-An ZhangJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Laboratory of Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou 215123, P.R. China.
Qiya XuJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Laboratory of Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou 215123, P.R. China.
Hang ZhengJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Laboratory of Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou 215123, P.R. China.
Guang-Yin XuJiangsu Key Laboratory of Translational Research and Therapy for Neuro-Psycho-Diseases, Laboratory of Translational Pain Medicine, Institute of Neuroscience, Soochow University, Suzhou 215123, P.R. China.
Soochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The central mechanisms of visceral hypersensitivity remain largely unknown. It's reported that there are highest densities of TRPV1 labeled neurons within basolateral amygdala (BLA). The aim of this study was to explore the role and mechanisms of TRPV1 in BLA in development of visceral hypersensitivity. Visceral hypersensitivity was induced by neonatal maternal deprivation (NMD) and was quantified by abdominal withdrawal reflex. Expression of TRPV1 was determined by Western blot. The synaptic transmission of neurons in BLA was recorded by patch clamping. It was found that the expression of TRPV1 in BLA was significantly upregulated in NMD rats; glutamatergic synaptic activities in BLA were increased in NMD rats; application of capsazepine (TRPV1 antagonist) decreased glutamatergic synaptic activities of BLA neurons in NMD slices through a presynaptic mechanism; application of capsaicin (TRPV1 agonist) increased glutamatergic synaptic activities of BLA neurons in control slices through presynaptic mechanism without affecting GABAergic synaptic activities; microinjecting capsazepine into BLA significantly increased colonic distension threshold both in control and NMD rats. Our data suggested that upregulation of TRPV1 in BLA contributes to visceral hypersensitivity of NMD rats through enhancing excitation of BLA, thus identifying a potential target for treatment of chronic visceral pain.

Indexed as

Synaptic TransmissionAnimalsBasolateral Nuclear ComplexCapsaicinExcitatory Postsynaptic PotentialsHypersensitivityIn Vitro TechniquesMaleMaternal DeprivationPatch-Clamp TechniquesPyramidal CellsRatsRats, Sprague-DawleySynapsesTRPV Cation ChannelsUp-RegulationCapsaicincapsazepineTrpv1 protein, ratTRPV Cation Channels

Identifiers

PMID27364923
PMCPMC4929564
OpenAlexW2470750263

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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.