Evidence map›Paper›PMID 30118561›Full record

ArticleThe European journal of neuroscience2019

Cocaine self-administration is increased after frontal traumatic brain injury and associated with neuroinflammation.

Cole Vonder Haar, Jacqueline-Marie N Ferland, Sukhbir Kaur, Lara-Kirstie Riparip, Susanna Rosi, Catharine A Winstanley

Open access · greenAbstract read
In one paragraph

Article in The European journal of neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  7. Deletion ofFrontiers in pharmacology · 2023
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  9. Oral Enrichment of Streptococcus and its Role in Systemic Inflammation Related to Monocyte Activation in Humans with Cocaine Use Disorder.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022
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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

6 authors at 3 institutions in 2 countries.

Cole Vonder HaarInjury and Recovery Laboratory, Department of Psychology, West Virginia University, PO Box 6040, 53 Campus Drive, Morgantown, WV, 26505, USA.ORCID 0000-0001-7949-2068
Jacqueline-Marie N FerlandLaboratory of Molecular and Behavioural Neuroscience, University of British Columbia, 2215 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada.
Sukhbir KaurLaboratory of Molecular and Behavioural Neuroscience, University of British Columbia, 2215 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada.
Lara-Kirstie RiparipBrain and Spinal Injury Center, Departments of Physical Therapy Rehabilitation Science and Neurological Surgery, University of California San Francisco, San Francisco, CA, USA.
Susanna RosiBrain and Spinal Injury Center, Departments of Physical Therapy Rehabilitation Science and Neurological Surgery, University of California San Francisco, San Francisco, CA, USA.
Catharine A WinstanleyLaboratory of Molecular and Behavioural Neuroscience, University of British Columbia, 2215 Wesbrook Mall, Vancouver, BC, V6T 1Z3, Canada.
University of British Columbia · CAUniversity of California, San Francisco · USWest Virginia University · US

Funding

Contribution of infiltrating macrophages on synaptic function after TBIR21NS087458 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ROSI, SUSANNA · 2014 to 2015
$435k
Institute of Neurosciences, Mental Health and Addiction PJT-148631NINDS NIH HHS R21 NS087458NINDS NIH HHS R21NS087458
6 · The paper itself

Abstract

Traumatic brain injury (TBI) has been linked to the development of numerous psychiatric diseases, including substance use disorder. However, it can be difficult to ascertain from clinical data whether the TBI is cause or consequence of increased addiction vulnerability. Surprisingly few studies have taken advantage of animal models to investigate the causal nature of this relationship. In terms of a plausible neurobiological mechanism through which TBI could magnify the risk of substance dependence, numerous studies indicate that TBI can cause widespread disruption to monoaminergic signaling in striatal regions, and also increases neuroinflammation. In the current study, male Long-Evans rats received either a mild or severe TBI centered over the frontal cortex via controlled cortical impact, and were subsequently trained to self-administer cocaine over 10 6-hour sessions. At the end of the study, markers of striatal dopaminergic function, and levels of inflammatory cytokine levels in the frontal lobes, were assessed via western blot and multiplex ELISA, respectively. There was significantly higher cocaine intake in a subset of animals with either mild or severe TBI. However, many animals within both TBI groups failed to acquire self-administration. Principal components analysis suggested that both dopaminergic and neuroinflammatory proteins were associated with overall cocaine intake, yet only an inflammatory component was associated with acquisition of self-administration, suggesting neuroinflammation may make a more substantial contribution to the likelihood of drug-taking. Should neuroinflammation play a causal role in mediating TBI-induced addiction risk, anti-inflammatory therapy may reduce the likelihood of substance abuse in TBI populations.

Indexed as

AnimalsBrain Injuries, TraumaticCocaineDisease Models, AnimalFrontal LobeInflammationMaleRats, Long-EvansRats, Sprague-DawleySelf AdministrationCocainebrain injurycytokinedopaminepsychostimulantrat

Identifiers

PMID30118561
PMCPMC6517083
OpenAlexW2885956288

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.