Evidence map›Paper›PMID 24032718›Full record

ArticleJournal of neurochemistry2013

Intravenous nicotine injection induces rapid, experience-dependent sensitization of glutamate release in the ventral tegmental area and nucleus accumbens.

Magalie Lenoir, Eugene A Kiyatkin

Abstract read
In one paragraph

Article in Journal of neurochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 23% 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

18 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. A large-scale c-Fos brain mapping study on extinction of cocaine-primed reinstatement.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  3. NMDA Receptor Activation and CaNeurochemical research · 2023
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Neurobiological Considerations for Tobacco Use Disorder.Current behavioral neuroscience reports · 2018
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Molecular Mechanism: ERK Signaling, Drug Addiction, and Behavioral Effects.Progress in molecular biology and translational science · 2016
    Review
  16. Review
  17. Review
  18. Article
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

2 authors at 2 institutions in 1 country.

Magalie LenoirIn-Vivo Electrophysiology Unit, Behavioral Neuroscience Branch, National Institute on Drug Abuse - Intramural Research Program, National Institutes of Health, DHHS, Baltimore, Maryland, USA.
Eugene A Kiyatkin
National Institute on Drug Abuse · USNational Institutes of Health · US

Funding

Electrophysiological and electrochemical studues of addictive drugsZIADA000566 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI KIYATKIN, EUGENE A · 2010 to 2025
$10.1M
Intramural NIH HHS ZIA DA000566
6 · The paper itself

Abstract

Although numerous data suggest that glutamate (GLU) is involved in mediating the neural effects of nicotine, direct data on nicotine-induced changes in GLU release are still lacking. Here, we used high-speed amperometry with enzyme-based GLU and enzyme-free GLU-null biosensors to examine changes in extracellular GLU levels in the ventral tegmental area (VTA) and nucleus accumbens shell (NAcc) induced by intravenous nicotine in a low, behaviorally active dose (30 μg/kg) in freely moving rats. Using this approach, we found that the initial nicotine injection in drug-naive conditions induces rapid, transient, and relatively small GLU release (~ 90 nM; latency ~ 15 s, duration ~ 60 s) that is correlative in the VTA and NAcc. Following subsequent nicotine injections within the same session, this phasic GLU release was supplemented by stronger tonic increases in GLU levels (100-300 nM) that paralleled increases in drug-induced locomotor activation. GLU responses induced by repeated nicotine injections were more phasic and stronger in the NAcc than in VTA. Therefore, GLU is phasically released within the brain's reinforcement circuit following intravenous nicotine administration. Robust enhancement of nicotine-induced GLU responses following repeated injections suggests this change as an important mediator of sensitized behavioral and neural effects of nicotine. By using high-speed amperometry with glutamate (GLU) biosensors, we show that i.v. nicotine at a low, behaviorally relevant dose induces rapid GLU release in the NAcc and VTA that is enhanced following repeated drug injections. This is the first study reporting second-scale fluctuations in extracellular GLU levels induced by nicotine in two critical structures of the motivation-reinforcement circuit and rapid sensitization of GLU responses coupled with locomotor sensitization.

Indexed as

AnimalsBiosensing TechniquesDose-Response Relationship, DrugGlutamineInjections, IntravenousLocomotionMaleNicotineNucleus AccumbensRatsRats, Long-EvansVentral Tegmental AreaGlutamineNicotineelectrochemistryenzyme-based glutamate biosensorsexperience-dependent neuroplasticity of glutamate neurotransmissionglutamate release

Identifiers

PMID24032718
PMCPMC4529058
OpenAlexW2084634246

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.