Evidence map›Paper›PMID 26972828›Full record

ArticleNeuropharmacology2016

Peripheral ammonia and blood brain barrier structure and function after methamphetamine.

Nicole A Northrop, Laura E Halpin, Bryan K Yamamoto

Open access · greenAbstract read
In one paragraph

Article in Neuropharmacology, 2016. 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
2.7field-weighted citation impact, top 11% 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, 41 citations in OpenAlex.

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  9. Astrocyte-derived TNF and glutamate critically modulate microglia activation by methamphetamine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
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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

3 authors at 2 institutions in 1 country.

Nicole A NorthropDepartment of Neurosciences, University of Toledo College of Medicine, 3000 Arlington Ave., Toledo, OH 43614, USA.
Laura E HalpinDepartment of Neurosciences, University of Toledo College of Medicine, 3000 Arlington Ave., Toledo, OH 43614, USA.
Bryan K YamamotoDepartment of Pharmacology and Toxicology, Indiana University School of Medicine, 635 Barnhill Drive, Indianapolis, IN 46202, USA. Electronic address: brkyama@iu.edu.
University of Toledo · USIndiana University School of Medicine

Funding

METHAMPHETAMINE TOXICITY AND CORTICOSTRIATAL GLUTAMATER01DA007606 · NIDA · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI YAMAMOTO, BRYAN K · 1992 to 2016
$5.1M
Methamphetamine, Stress and Brain EndotheliumR01DA035499 · NIDA · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI YAMAMOTO, BRYAN K · 2013 to 2017
$2.2M
NIDA NIH HHS R01 DA007606NIDA NIH HHS R01 DA035499
6 · The paper itself

Abstract

An effect of the widely abuse psychostimulant, methamphetamine (Meth), is blood-brain-barrier (BBB) disruption; however, the mechanism by which Meth causes BBB disruption remains unclear. Recently it has been shown that Meth produces liver damage and consequent increases in plasma ammonia. Ammonia can mediate oxidative stress and inflammation, both of which are known to cause BBB disruption. Therefore, the current studies examined the role of peripheral ammonia in Meth-induced disruption of BBB structure and function. A neurotoxic Meth regimen (10 mg/kg, ip, q 2 h, ×4) administered to rats increased plasma ammonia and active MMP-9 in the cortex 2 h after the last Meth injection, compared to saline treated rats. At 24 h after Meth treatment, decreased immunoreactivity of BBB structural proteins, occludin and claudin-5, and increased extravasation of 10,000 Da FITC-dextran were observed, as compared to saline controls. Pretreatment with lactulose (5.3 g/kg, po, q 12 h), a drug that remains in the lumen of the intestine and promotes ammonia excretion, prevented the Meth-induced increases in plasma ammonia. These results were paralleled by the prevention of decreases in BBB structural proteins, increases in extravasation of 10,000 Da FITC-dextran and increases in active MMP-9. The results indicate that Meth-induced increases in ammonia produce BBB disruption and suggest that MMP-9 activation mediates the BBB disruption. These findings identify a novel mechanism of Meth-induced BBB disruption that is mediated by plasma ammonia and are the first to identify a peripheral contribution to Meth-induced BBB disruption.

Indexed as

AmmoniaAnimalsBlood-Brain BarrierCapillariesCapillary PermeabilityCentral Nervous System StimulantsCerebral CortexClaudin-5Disease Models, AnimalFeverGastrointestinal AgentsLactuloseMaleMatrix Metalloproteinase 9MethamphetamineOccludinAmmoniaCentral Nervous System StimulantsClaudin-5Cldn5 protein, ratGastrointestinal AgentsLactuloseMatrix Metalloproteinase 9MethamphetamineMmp9 protein, ratOccludinOcln protein, ratAmmoniaBlood-brain barrierMethamphetamine

Identifiers

PMID26972828
PMCPMC5264515
OpenAlexW2301983880

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.