Evidence map›Paper›PMID 27306143›Full record

ArticleJournal of neurotrauma2017

Early and Persistent Dendritic Hypertrophy in the Basolateral Amygdala following Experimental Diffuse Traumatic Brain Injury.

Ann N Hoffman, Pooja R Paode, Hazel G May, J Bryce Ortiz, Salma Kemmou, Jonathan Lifshitz, Cheryl D Conrad, Theresa Currier Thomas

Abstract read
In one paragraph

Article in Journal of neurotrauma, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-weighted citation impact, top 7% 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

36 citing papers in PubMed, 49 citations in OpenAlex.

  1. Review
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  6. Repetitive mild traumatic brain injuries in children of abuse.Annals of the Child Neurology Society · 2023
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  16. Drosophila as a model to explore secondary injury cascades after traumatic brain injury.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021
    Review
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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

8 authors at 3 institutions in 2 countries.

Ann N Hoffman1 Department of Psychology, Arizona State University , Tempe, Arizona.
Pooja R Paode1 Department of Psychology, Arizona State University , Tempe, Arizona.
Hazel G May2 Department of Child Health, University of Arizona College of Medicine-Phoenix , Phoenix, Arizona.
J Bryce Ortiz1 Department of Psychology, Arizona State University , Tempe, Arizona.
Salma Kemmou1 Department of Psychology, Arizona State University , Tempe, Arizona.
Jonathan Lifshitz1 Department of Psychology, Arizona State University , Tempe, Arizona.
Cheryl D Conrad1 Department of Psychology, Arizona State University , Tempe, Arizona.
Theresa Currier Thomas2 Department of Child Health, University of Arizona College of Medicine-Phoenix , Phoenix, Arizona.
Arizona State University · USPhoenix Children's Hospital · USPhoenix VA Health Care System · US

Funding

Graduate and Undergraduate Training in Biomedicine at ASUR25GM099650 · NIGMS · ARIZONA STATE UNIVERSITY-TEMPE CAMPUS · PI NEWFELD, STUART J · 2012 to 2015
$2.2M
Neural circuit disruption by diffuse brain injury: basis for morbidity & therapyR01NS065052 · NINDS · UNIVERSITY OF KENTUCKY · PI LIFSHITZ, JONATHAN · 2010 to 2014
$1.7M
NIGMS NIH HHS R25 GM099650NINDS NIH HHS R01 NS065052
6 · The paper itself

Abstract

In the pathophysiology of traumatic brain injury (TBI), the amygdala remains understudied, despite involvement in processing emotional and stressful stimuli associated with anxiety disorders, such as post-traumatic stress disorder (PTSD). Because the basolateral amygdala (BLA) integrates inputs from sensory and other limbic structures coordinating emotional learning and memory, injury-induced changes in circuitry may contribute to psychiatric sequelae of TBI. This study quantified temporal changes in dendritic complexity of BLA neurons after experimental diffuse TBI, modeled by midline fluid percussion injury. At post-injury days (PIDs) 1, 7, and 28, brain tissue from sham and brain-injured adult, male rats was processed for Golgi, glial fibrillary acidic protein (GFAP), or silver stain and analyzed to quantify BLA dendritic branch intersections, activated astrocytes, and regional neuropathology, respectively. Compared to sham, brain-injured rats at all PIDs showed enhanced dendritic branch intersections in both pyramidal and stellate BLA neuronal types, as evidenced by Sholl analysis. GFAP staining in the BLA was significantly increased at PID1 and 7 in comparison to sham. However, the BLA was relatively spared from neuropathology, demonstrated by an absence of argyrophilic accumulation over time, in contrast to other brain regions. These data suggest an early and persistent enhancement of dendritic complexity within the BLA after a single diffuse TBI. Increased dendritic complexity would alter information processing into and through the amygdala, contributing to emotional symptoms post-TBI, including PTSD.

Indexed as

AnimalsBasolateral Nuclear ComplexBrain Injuries, DiffuseBrain Injuries, TraumaticDendritesHypertrophyMaleRatsRats, Sprague-DawleyTime Factorsamygdalacomorbidityplasticitypost-traumatic stress disordertraumatic brain injury

Identifiers

PMID27306143
PMCPMC5198057
OpenAlexW2434877139

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.