Evidence map›Paper›PMID 21939393›Full record

ArticleJournal of neurotrauma2012

Hypersensitive glutamate signaling correlates with the development of late-onset behavioral morbidity in diffuse brain-injured circuitry.

Theresa Currier Thomas, Jason M Hinzman, Greg A Gerhardt, Jonathan Lifshitz

Open access · greenAbstract read
In one paragraph

Article in Journal of neurotrauma, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

44 citing papers in PubMed, 59 citations in OpenAlex.

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  6. Real-time in vivo thoracic spinal glutamate sensing during myocardial ischemia.American journal of physiology. Heart and circulatory physiology · 2023
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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

4 authors at 1 institution in 1 country.

Theresa Currier ThomasSpinal Cord & Brain Injury Research Center, University of Kentucky College of Medicine, Lexington, Kentucky, USA.
Jason M Hinzman
Greg A Gerhardt
Jonathan Lifshitz
University of Kentucky · US

Funding

UK Spinal Cord &Brain Injury Research Center Core GrantP30NS051220 · NINDS · UNIVERSITY OF KENTUCKY · PI HALL, EDWARD D. · 2005 to 2015
$6.4M
THE MOLECULAR AND CELLULAR BASIS OF BRAIN AGINGT32AG000242 · NIA · UNIVERSITY OF KENTUCKY · PI GERHARDT, GREG A. · 1994 to 2013
$3.4M
Neural circuit disruption by diffuse brain injury: basis for morbidity & therapyR01NS065052 · NINDS · UNIVERSITY OF KENTUCKY · PI LIFSHITZ, JONATHAN · 2010 to 2014
$1.7M
Inhibition of synaptogenesis mitigates late-onset post-traumatic morbidity in ratR03NS077098 · NINDS · UNIVERSITY OF ARIZONA · PI LIFSHITZ, JONATHAN · 2012 to 2013
$149k
NIA NIH HHS T32 AG000242NINDS NIH HHS P30 NS051220
6 · The paper itself

Abstract

In diffuse brain-injured rats, robust sensory sensitivity to manual whisker stimulation develops over 1 month post-injury, comparable to agitation expressed by brain-injured individuals with overstimulation. In the rat, whisker somatosensation relies on thalamocortical glutamatergic relays between the ventral posterior medial (VPM) thalamus and barrel fields of somatosensory cortex (S1BF). Using novel glutamate-selective microelectrode arrays coupled to amperometry, we test the hypothesis that disrupted glutamatergic neurotransmission underlies the whisker sensory sensitivity associated with diffuse brain injury. We report hypersensitive glutamate neurotransmission that parallels and correlates with the development of post-traumatic sensory sensitivity. Hypersensitivity is demonstrated by significant 110% increases in VPM extracellular glutamate levels, and 100% increase in potassium-evoked glutamate release in the VPM and S1BF, with no change in glutamate clearance. Further, evoked glutamate release showed 50% greater sensitivity to a calcium channel antagonist in brain-injured over uninjured VPM. In conjunction with no changes in glutamate transporter gene expression and exogenous glutamate clearance efficiency, these data support a presynaptic origin for enduring post-traumatic circuit alterations. In the anatomically-distinct whisker circuit, the injury-induced functional alterations correlate with the development of late-onset behavioral morbidity. Effective therapies to modulate presynaptic glutamate function in diffuse-injured circuits may translate into improvements in essential brain function and behavioral performance in other brain-injured circuits in rodents and in humans.

Indexed as

Afferent PathwaysAnimalsBehavior, AnimalBrain InjuriesDiffuse Axonal InjuryDisease Models, AnimalGlutamic AcidHyperesthesiaMaleRatsRats, Sprague-DawleySignal TransductionTime FactorsGlutamic Acid

Identifiers

PMID21939393
PMCPMC3261793
OpenAlexW1975016302

What OpenQuestion holds

Textmetadata
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.