Evidence map›Paper›PMID 34710467›Full record

ReviewNeuropharmacology2022

Reciprocal midbrain-extended amygdala circuit activity in preclinical models of alcohol use and misuse.

Elizabeth M Avegno, Nicholas W Gilpin

Abstract readReview
In one paragraph

Review in Neuropharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
–field-weighted citation impact
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

9 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Chronic alcohol withdrawal-associated increases in VTAAdvances in drug and alcohol research · 2025
    Article
  6. Neural Circuitries and Alcohol Use Disorder: Cutting Corners in the Cycle.Current topics in behavioral neurosciences · 2025
    Review
  7. Article
  8. Article
  9. Neurotensin and Alcohol Use Disorders: Towards a Pharmacological Treatment.International journal of molecular sciences · 2023
    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.

Elizabeth M AvegnoDepartment of Physiology, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA; Alcohol and Drug Abuse Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA. Electronic address: eavegn@lsuhsc.edu.
Nicholas W GilpinDepartment of Physiology, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA; Alcohol and Drug Abuse Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA; Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA; Southeast Louisiana VA Healthcare System (SLVHCS), New Orleans, LA, USA.

Funding

Role of Neuropeptides in Stress-Induced Escalation of Alcohol DrinkingR01AA023305 · NIAAA · LSU HEALTH SCIENCES CENTER · PI GILPIN, NICHOLAS WARREN · 2014 to 2024
$3.7M
8/8 NADIA U01 Long-Term Effects of Adolescent Alcohol on PainU01AA028709 · NIAAA · LSU HEALTH SCIENCES CENTER · PI GILPIN, NICHOLAS WARREN, WILLS, TIFFANY A · 2020 to 2024
$1.8M
Targeting Melanocortin-4 Receptors to Reduce Pain in U.S. VeteransI01BX003451 · VA · SOUTHEAST LOUISIANA VETERANS HEALTH CARE · PI GILPIN, NICHOLAS WARREN · 2017 to 2025
–
BLRD VA I01 BX003451NIAAA NIH HHS R01 AA023305NIAAA NIH HHS U01 AA028709
6 · The paper itself

Abstract

Alcohol dependence is characterized by a shift in motivation to consume alcohol from positive reinforcement (i.e., increased likelihood of future alcohol drinking based on its rewarding effects) to negative reinforcement (i.e., increased likelihood of future alcohol drinking based on alcohol-induced reductions in negative affective symptoms, including but not limited to those experienced during alcohol withdrawal). The neural adaptations that occur during this transition are not entirely understood. Mesolimbic reinforcement circuitry (i.e., ventral tegmental area [VTA] neurons) is activated during early stages of alcohol use, and may be involved in the recruitment of brain stress circuitry (i.e., extended amygdala) during the transition to alcohol dependence, after chronic periods of high-dose alcohol exposure. Here, we review the literature regarding the role of canonical brain reinforcement (VTA) and brain stress (extended amygdala) systems, and the connections between them, in acute, sub-chronic, and chronic alcohol response. Particular emphasis is placed on preclinical models of alcohol use.

Indexed as

Adaptation, PsychologicalAlcohol DrinkingAlcoholismAmygdalaAnimalsHumansMesencephalonMotivationNeural PathwaysReinforcement, PsychologyVentral Tegmental AreaAddictionAlcoholBed nucleus of stria terminalisCentral amygdalaExtended amygdalaNucleus accumbensVentral tegmental area

Identifiers

PMID34710467
PMCPMC8627447

What OpenQuestion holds

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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.