Evidence map›Paper›PMID 30535261›Full record

ArticleThe international journal of neuropsychopharmacology2019

Neuroinflammation Contributes to High Salt Intake-Augmented Neuronal Activation and Active Coping Responses to Acute Stress.

T Lee Gilman, Nathan C Mitchell, Lynette C Daws, Glenn M Toney

Open access · goldAbstract read
In one paragraph

Article in The international journal of neuropsychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 44% 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

10 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
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  9. Article
  10. High Salt Intake Lowers Behavioral Inhibition.Frontiers in behavioral neuroscience · 2019
    Article
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

4 authors at 1 institution in 1 country.

T Lee GilmanDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Nathan C MitchellDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Lynette C DawsDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
Glenn M ToneyDepartment of Cellular and Integrative Physiology, University of Texas Health Science Center at San Antonio, San Antonio, Texas.
The University of Texas Health Science Center at San Antonio · US

Funding

PATHOBIOLOGY OF OCCLUSIVE VASCULAR DISEASET32HL007446 · NHLBI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Jean Chrisostome Bopassa · 1985 to 2026
$8.9M
Role of the serotonin transporter and organic cation transporter 3 in serotonergic modulation of emotion-regulating circuitryR01MH093320 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DAWS, LYNETTE C, TONEY, GLENN M · 2012 to 2023
$6.3M
Training in Drug Abuse Research: Behavior and NeurobiologyT32DA031115 · NIDA · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CHARLES P FRANCE · 2011 to 2026
$5.2M
Age-related differences in serotonin clearance: novel targets for antidepressantsR01MH106978 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI DAWS, LYNETTE C · 2015 to 2019
$2.5M
National Institute on Drug Abuse T32 DA031115NHLBI NIH HHS T32 HL007446NIMH NIH HHS R01 MH093320NIMH NIH HHS R01 MH106978
6 · The paper itself

Abstract

High dietary salt intake increases risk of stress-related neuropsychiatric disorders. Here, we explored the contribution of high dietary salt intake-induced neuroinflammation in key stress-responsive brain regions, the hypothalamic paraventricular nucleus and basolateral amygdala, in promoting exaggerated neuronal activation and coping behaviors in response to acute psychogenic stress. Mice that underwent high dietary salt intake exhibited increased active stress coping behaviors during and after an acute swim stress, and these were reduced by concurrent administration of minocycline, an inhibitor of microglial activation, without affecting body fluid hyperosmolality caused by high dietary salt intake. Moreover, minocycline attenuated high dietary salt intake-induced increases of paraventricular nucleus tumor necrosis factor-α, activated microglia (ionized calcium-binding adaptor molecule 1), and acute swim stress-induced neuronal activation (c-Fos). In the basolateral amygdala, similar effects were observed on ionized calcium-binding adaptor molecule 1+ and c-Fos+ counts, but not tumor necrosis factor-α levels. These data indicate that high dietary salt intake promotes neuroinflammation, increasing recruitment of neurons in key stress-associated brain regions and augmenting behavioral hyper-responsivity to acute psychological stress.

Indexed as

Adaptation, PsychologicalBasolateral Nuclear ComplexBrainInflammationMicrogliaParaventricular Hypothalamic NucleusStress, PsychologicalAnimalsAnti-Inflammatory AgentsBehavior, AnimalDisease Models, AnimalMaleMiceMice, Inbred C57BLMinocyclineSodium Chloride, DietaryAnti-Inflammatory AgentsMinocyclineSodium Chloride, Dietary

Identifiers

PMID30535261
PMCPMC6368371
OpenAlexW2903862287

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
Read underepoch 390

Registered trials

None linked

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.