Evidence map›Paper›PMID 27525447›Full record

ArticleACS chemical neuroscience2016

Frontal Traumatic Brain Injury in Rats Causes Long-Lasting Impairments in Impulse Control That Are Differentially Sensitive to Pharmacotherapeutics and Associated with Chronic Neuroinflammation.

Cole Vonder Haar, Frederick C W Lam, Wendy K Adams, Lara-Kirstie Riparip, Sukhbir Kaur, Michael Muthukrishna, Susanna Rosi, Catharine A Winstanley

Open access · greenAbstract read
In one paragraph

Article in ACS chemical neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Basal forebrain-lateral habenula inputs and control of impulsive behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
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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.

Cole Vonder Haar
Frederick C W Lam
Wendy K Adams
Lara-Kirstie RiparipBrain and Spinal Injury Center, Departments of Physical Therapy Rehabilitation Science and Neurological Surgery, University of California, San Francisco , San Francisco, California 94143, United States.
Sukhbir Kaur
Michael Muthukrishna
Susanna RosiBrain and Spinal Injury Center, Departments of Physical Therapy Rehabilitation Science and Neurological Surgery, University of California, San Francisco , San Francisco, California 94143, United States.
Catharine A Winstanley
University of British Columbia · CAUniversity of California, San Francisco · USNeurological Surgery · US

Funding

Contribution of infiltrating macrophages on synaptic function after TBIR21NS087458 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSI, SUSANNA · 2014 to 2015
$435k
CIHRNINDS NIH HHS R21 NS087458
6 · The paper itself

Abstract

Traumatic brain injury (TBI) affects millions yearly, and is increasingly associated with chronic neuropsychiatric symptoms. We assessed the long-term effects of different bilateral frontal controlled cortical impact injury severities (mild, moderate, and severe) on the five-choice serial reaction time task, a paradigm with relatively independent measurements of attention, motor impulsivity, and motivation. Moderately- and severely injured animals exhibited impairments across all cognitive domains that were still evident 14 weeks postinjury, while mild-injured animals only demonstrated persistent deficits in impulse control. However, recovery of function varied considerably between subjects such that some showed no impairment ("TBI-resilient"), some demonstrated initial deficits that recovered ("TBI-vulnerable"), and some never recovered ("chronically-impaired"). Three clinically relevant treatments for impulse-control or TBI, amphetamine, atomoxetine, and amantadine, were assessed for efficacy in treating injury-induced deficits. Susceptibility to TBI affected the response to pharmacological challenge with amphetamine. Whereas sham and TBI-resilient animals showed characteristic impairments in impulse control at higher doses, amphetamine had the opposite effect in chronically impaired rats, improving task performance. In contrast, atomoxetine and amantadine reduced premature responding but increased omissions, suggesting psychomotor slowing. Analysis of brain tissue revealed that generalized neuroinflammation was associated with impulsivity even when accounting for the degree of brain damage. This is one of the first studies to characterize psychiatric-like symptoms in experimental TBI. Our data highlight the importance of testing pharmacotherapies in TBI models in order to predict efficacy, and suggest that neuroinflammation may represent a treatment target for impulse control problems following injury.

Indexed as

Acute DiseaseAdrenergic Uptake InhibitorsAmantadineAmphetamineAnimalsAtomoxetine HydrochlorideBrain Injuries, TraumaticCentral Nervous System StimulantsChronic DiseaseDisease Models, AnimalDisease ProgressionDisruptive, Impulse Control, and Conduct DisordersDopamine AgentsFrontal LobeMaleMotor ActivityAdrenergic Uptake InhibitorsAmantadineAmphetamineAtomoxetine HydrochlorideCentral Nervous System StimulantsDopamine AgentsamphetamineControlled cortical impactcytokineimpulsivityprelimbic

Identifiers

PMID27525447
PMCPMC9487719
OpenAlexW2509413750

What OpenQuestion holds

Textmetadata
LicenceTDM
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.