Evidence map›Paper›PMID 28802560›Full record

ArticleExperimental neurology2017

Traumatic brain injuries during development disrupt dopaminergic signaling.

Kate Karelina, Kristopher R Gaier, Zachary M Weil

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

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  15. Alcohol Use Disorder and Traumatic Brain Injury.Alcohol research : current reviews · 2018
    Review
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

3 authors at 1 institution in 1 country.

Kate KarelinaDepartment of Neuroscience, Group in Behavioral Neuroendocrinology, Center for Brain and Spinal Cord Repair, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA. Electronic address: Ekaterina.karelina@osumc.edu.
Kristopher R GaierDepartment of Neuroscience, Group in Behavioral Neuroendocrinology, Center for Brain and Spinal Cord Repair, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
Zachary M WeilDepartment of Neuroscience, Group in Behavioral Neuroendocrinology, Center for Brain and Spinal Cord Repair, The Ohio State University Wexner Medical Center, Columbus, OH 43210, USA.
The Ohio State University Wexner Medical Center · US

Funding

Ohio State Neuroscience Centr CoreP30NS045758 · NINDS · OHIO STATE UNIVERSITY · PI OBRIETAN, KARL H · 2004 to 2015
$7.7M
Ohio State University Neuroscience Center Core-Core EP30NS104177 · NINDS · OHIO STATE UNIVERSITY · PI BROWN, ANTHONY · 2017 to 2020
$1.9M
NINDS NIH HHS P30 NS045758NINDS NIH HHS P30 NS104177
6 · The paper itself

Abstract

Traumatic brain injuries (TBI) sustained during peri-adolescent development produce lasting neuro-behavioral changes that render individuals at an increased risk for developing substance abuse disorders. Experimental and clinical evidence of a prolonged period of hypodopaminergia after TBI have been well documented, but the effect of juvenile TBI on dopaminergic dysfunction and its relationship with substance abuse have not been investigated. In order to determine the effect of juvenile brain injury on dopaminergic signaling, female mice were injured at 21days of age and then beginning seven weeks later were assessed for behavioral sensitization to amphetamine, a drug that increases synaptic dopamine availability. Together with a histological analysis of tyrosine hydroxylase, dopamine transporter, and dopamine D2 receptor expression, our data are indicative of a persistent state of hypodopaminergia well into adulthood after a juvenile TBI. Further, mice that sustained a juvenile TBI exhibited a significantly reduced activation of cFos in the urocortin-positive cells of the Edinger-Westphal nucleus in response to ethanol administration. Taken together, these data provide strong evidence for the vulnerability of juveniles to the development of lasting neuro-behavioral problems following TBI, and indicate a role of injury-induced hypodopaminergia as a risk factor for substance abuse later in life.

Indexed as

Age FactorsAnimalsBrainBrain Injuries, TraumaticDopamineDopamine Plasma Membrane Transport ProteinsDopaminergic NeuronsFemaleLocomotionMiceReceptors, Dopamine D2Tyrosine 3-MonooxygenaseDopamineDopamine Plasma Membrane Transport ProteinsReceptors, Dopamine D2Tyrosine 3-MonooxygenaseAlcoholDevelopmentDopamineHypodopaminergiaTraumatic brain injury

Identifiers

PMID28802560
PMCPMC6033277
OpenAlexW2742263201

What OpenQuestion holds

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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.