Evidence map›Paper›PMID 21762181›Full record

ReviewAlcoholism, clinical and experimental research2012

Neuroadaptations in adenosine receptor signaling following long-term ethanol exposure and withdrawal.

Tracy R Butler, Mark A Prendergast

Abstract readReview
In one paragraph

Review in Alcoholism, clinical and experimental research, 2012. 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
2.8field-weighted citation impact, top 12% 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, 33 citations in OpenAlex.

  1. Trial
  2. Review
  3. Effect of caffeine on alcohol drinking in mice.Alcohol (Fayetteville, N.Y.) · 2021
    Article
  4. Input-selective adenosine AScientific reports · 2021
    Article
  5. Indirect Medium Spiny Neurons in the Dorsomedial Striatum Regulate Ethanol-Containing Conditioned Reward Seeking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  6. Article
  7. Review
  8. Article
  9. Critical needs in drug discovery for cessation of alcohol and nicotine polysubstance abuse.Progress in neuro-psychopharmacology & biological psychiatry · 2016
    Review
  10. Article
  11. Can energy drinks increase the desire for more alcohol?Advances in nutrition (Bethesda, Md.) · 2015
    Review
  12. Review
  13. Review
  14. Review
  15. Caffeinated Alcoholic Beverages - An Emerging Trend in Alcohol Abuse.Journal of addiction research & therapy · 2013
    Article
  16. Sex differences in neuroadaptation to alcohol and withdrawal neurotoxicity.Pflugers Archiv : European journal of physiology · 2013
    Review
  17. Article
  18. 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

2 authors at 1 institution in 1 country.

Tracy R ButlerDepartment of Psychology, Spinal Cord and Brain Injury Research Center, University of Kentucky, Lexington, USA. tracyrbutler@uky.edu
Mark A Prendergast
Albert B. Chandler Hospital · US

Funding

Hippocamppal neurotoxicity induced by ethanol withdrawalR01AA013388 · NIAAA · UNIVERSITY OF KENTUCKY · PI PRENDERGAST, MARK A · 2003 to 2013
$2.8M
Adenosine Receptors and Ethanol WithdrawalF31AA018588 · NIAAA · UNIVERSITY OF KENTUCKY · PI BUTLER, TRACY RENEE · 2009 to 2010
$54k
NIAAA NIH HHS F31 AA018588NIAAA NIH HHS R01 AA013388
6 · The paper itself

Abstract

Ethanol affects the function of neurotransmitter systems, resulting in neuroadaptations that alter neural excitability. Adenosine is one such receptor system that is changed by ethanol exposure. The current review is focused on the A(1) and the A(2A) receptor subtypes in the context of ethanol-related neuroadaptations and ethanol withdrawal because these subtypes (i) are activated by basal levels of adenosine, (ii) have been most well-studied for their role in neuroprotection and ethanol-related phenomena, and (iii) are the primary site of action for caffeine in the brain, a substance commonly ingested with ethanol. It is clear that alterations in adenosinergic signaling mediate many of the effects of acute ethanol administration, particularly with regard to motor function and sedation. Further, prolonged ethanol exposure has been shown to produce adaptations in the cell surface expression or function of both A(1) and the A(2A) receptor subtypes, effects that likely promote neuronal excitability during ethanol withdrawal. As a whole, these findings demonstrate a significant role for ethanol-induced adaptations in adenosine receptor signaling that likely influence neuronal function, viability, and relapse to ethanol intake following abstinence.

Indexed as

Adaptation, PhysiologicalAdenosineAlcohol DrinkingAnimalsEthanolHumansReceptors, Purinergic P1Signal TransductionSubstance Withdrawal SyndromeTime FactorsAdenosineEthanolReceptors, Purinergic P1

Identifiers

PMID21762181
PMCPMC3256740
OpenAlexW1842804751

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.