Evidence map›Paper›PMID 29514102›Full record

ArticleCell reports2018

Cooperative CRF and α1 Adrenergic Signaling in the VTA Promotes NMDA Plasticity and Drives Social Stress Enhancement of Cocaine Conditioning.

Jorge Tovar-Díaz, Matthew B Pomrenze, Russell Kan, Bahram Pahlavan, Hitoshi Morikawa

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. The Formation and Function of the VTA Dopamine System.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Acute Stress Enhances Associative Learning via Dopamine Signaling in the Ventral Lateral Striatum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  14. Review
  15. αFrontiers in pharmacology · 2020
    Review
  16. Article
  17. Review
  18. Aqueous Extract of SemenEvidence-based complementary and alternative medicine : eCAM · 2018
    Article
  19. Review
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

5 authors at 1 institution in 1 country.

Jorge Tovar-DíazDepartment of Neuroscience, University of Texas at Austin, Austin, TX 78712, USA; Waggoner Center for Alcohol and Addiction Research, University of Texas at Austin, Austin, TX 78712, USA.
Matthew B PomrenzeDepartment of Neuroscience, University of Texas at Austin, Austin, TX 78712, USA; Waggoner Center for Alcohol and Addiction Research, University of Texas at Austin, Austin, TX 78712, USA; Institute for Neuroscience, University of Texas at Austin, Austin, TX 78712, USA. Electronic address: matt.pomrenze@utexas.edu.
Russell KanDepartment of Neuroscience, University of Texas at Austin, Austin, TX 78712, USA.
Bahram PahlavanDepartment of Neuroscience, University of Texas at Austin, Austin, TX 78712, USA; Waggoner Center for Alcohol and Addiction Research, University of Texas at Austin, Austin, TX 78712, USA.
Hitoshi MorikawaDepartment of Neuroscience, University of Texas at Austin, Austin, TX 78712, USA; Waggoner Center for Alcohol and Addiction Research, University of Texas at Austin, Austin, TX 78712, USA; Institute for Neuroscience, University of Texas at Austin, Austin, TX 78712, USA. Electronic address: morikawa@utexas.edu.
The University of Texas at Austin · US

Funding

Calcium Signaling in the Reward Circuit &Drug AddictionR01DA015687 · NIDA · UNIVERSITY OF TEXAS AUSTIN · PI MORIKAWA, HITOSHI · 2003 to 2013
$2.4M
Alcohol Action on Neurons in the Brain Reward CircuitR01AA015521 · NIAAA · UNIVERSITY OF TEXAS AT AUSTIN · PI MORIKAWA, HITOSHI · 2007 to 2017
$2.4M
NIAAA NIH HHS R01 AA015521NIDA NIH HHS R01 DA015687
6 · The paper itself

Abstract

Stressful events rapidly trigger activity-dependent synaptic plasticity, driving the formation of aversive memories. However, it remains unclear how stressful experience affects plasticity mechanisms to regulate appetitive learning, such as intake of addictive drugs. Using rats, we show that corticotropin-releasing factor (CRF) and α1 adrenergic receptor (α1AR) signaling enhance the plasticity of NMDA-receptor-mediated glutamatergic transmission in ventral tegmental area (VTA) dopamine (DA) neurons through distinct effects on inositol 1,4,5-triphosphate (IP

Indexed as

Calcium SignalingNeuronal PlasticityAnimalsCocaineConditioning, PsychologicalCorticotropin-Releasing HormoneDopaminergic NeuronsInositol 1,4,5-TrisphosphateLearningLong-Term PotentiationMaleN-MethylaspartateNorepinephrinePhenylephrineRats, Sprague-DawleyReceptors, Adrenergic, alpha-1CocaineCorticotropin-Releasing HormoneInositol 1,4,5-TrisphosphateN-MethylaspartateNorepinephrinePhenylephrineReceptors, Adrenergic, alpha-1Ca(2+)cocaineCRFdopamine neuronIP(3)reward learningstressVTAα1AR

Identifiers

PMID29514102
PMCPMC5877815
OpenAlexW2790968059

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.