Evidence map›Paper›PMID 24165886›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2014

Ammonia mediates methamphetamine-induced increases in glutamate and excitotoxicity.

Laura E Halpin, Nicole A Northrop, Bryan K Yamamoto

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 1 pooled it
1.7field-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

35 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
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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 1 institution in 1 country.

Laura E HalpinDepartment of Neurosciences, University of Toledo College of Medicine, Toledo, OH, USA.
Nicole A NorthropDepartment of Neurosciences, University of Toledo College of Medicine, Toledo, OH, USA.
Bryan K YamamotoDepartment of Neurosciences, University of Toledo College of Medicine, Toledo, OH, USA.
University of Toledo · US

Funding

METHAMPHETAMINE TOXICITY AND CORTICOSTRIATAL GLUTAMATER01DA007606 · NIDA · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI YAMAMOTO, BRYAN K · 1992 to 2016
$5.1M
NIDA NIH HHS DA007606NIDA NIH HHS R01 DA007606
6 · The paper itself

Abstract

Ammonia has been identified to have a significant role in the long-term damage to dopamine and serotonin terminals produced by methamphetamine (METH), but how ammonia contributes to this damage is unknown. Experiments were conducted to identify whether increases in brain ammonia affect METH-induced increases in glutamate and subsequent excitotoxicity. Increases in striatal glutamate were measured using in vivo microdialysis. To examine the role of ammonia in mediating changes in extracellular glutamate after METH exposure, lactulose was used to decrease plasma and brain ammonia. Lactulose is a non-absorbable disaccharide, which alters the intestinal lumen through multiple mechanisms that lead to the increased peripheral excretion of ammonia. METH caused a significant increase in extracellular glutamate that was prevented by lactulose. Lactulose had no effect on METH-induced hyperthermia. To determine if ammonia contributed to excitotoxicity, the effect of METH and lactulose treatment on calpain-mediated spectrin proteolysis was measured. METH significantly increased calpain-specific spectrin breakdown products, and this increase was prevented with lactulose treatment. To examine if ammonia-induced increases in extracellular glutamate were mediated by excitatory amino-acid transporters, the reverse dialysis of ammonia, the glutamate transporter inhibitor, DL-threo-β-benzyloxyaspartic acid (TBOA), or the combination of the two directly into the striatum of awake, freely moving rats was conducted. TBOA blocked the increases in extracellular glutamate produced by the reverse dialysis of ammonia. These findings demonstrate that ammonia mediates METH-induced increases in extracellular glutamate through an excitatory amino-acid transporter to cause excitotoxicity.

Indexed as

AmmoniaAnimalsAspartic AcidBody TemperatureBrainCalpainCentral Nervous System StimulantsDose-Response Relationship, DrugDrug Administration RoutesGlial Fibrillary Acidic ProteinGlutamic AcidLactuloseMaleMethamphetamineMolecular WeightRatsAmmoniaAspartic AcidbenzyloxyaspartateCalpainCentral Nervous System StimulantsGlial Fibrillary Acidic ProteinGlutamic AcidLactuloseMethamphetamineSpectrin

Identifiers

PMID24165886
PMCPMC3924538
OpenAlexW2068880088

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.