Evidence map›Paper›PMID 22982568›Full record

ArticleNeuropharmacology2013

Thalamic glutamatergic afferents into the rat basolateral amygdala exhibit increased presynaptic glutamate function following withdrawal from chronic intermittent ethanol.

Daniel T Christian, Nancy J Alexander, Marvin R Diaz, Brian A McCool

Abstract read
In one paragraph

Article in Neuropharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
1.9field-weighted citation impact, top 16% 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

40 citing papers in PubMed, 51 citations in OpenAlex.

  1. Cannabidiol mitigates alcohol dependence and withdrawal with neuroprotective effects in the basolateral amygdala and striatum.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Synaptic Effects Induced by Alcohol.Current topics in behavioral neurosciences · 2025
    Review
  3. Review
  4. Modulation of neuronal excitability by binge alcohol drinking.Frontiers in molecular neuroscience · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Medial prefrontal cortex neuropeptide Y modulates binge-like ethanol consumption in C57BL/6J mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Article
  13. Review
  14. Review
  15. Article
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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

4 authors at 1 institution in 1 country.

Daniel T ChristianDepartment of Physiology and Pharmacology, Wake Forest School of Medicine, Winston-Salem, NC, USA.
Nancy J Alexander
Marvin R Diaz
Brian A McCool
Wake Forest University · US

Funding

MULTI-DISCIPLINARY TRAINING IN THE BIOLOGY OF ALCOHOLISMT32AA007565 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI BRIAN A MCCOOL · 1994 to 2026
$10.1M
The Ethanol - Anxiety Interaction: Cellular MechanismsR01AA014445 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCOOL, BRIAN A · 2004 to 2023
$5.2M
Withdrawal-Stress, Anxiety, and Amygdala NeurophysiologyU01AA020942 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCOOL, BRIAN A · 2012 to 2016
$911k
NIAAA NIH HHS R01 AA014445NIAAA NIH HHS T32 AA007565NIAAA NIH HHS U01 AA020942
6 · The paper itself

Abstract

Amygdala glutamatergic neurotransmission regulates withdrawal induced anxiety-like behaviors following chronic ethanol exposure. The lateral/basolateral amygdala receives multiple glutamatergic projections that contribute to overall amygdala function. Our lab has previously shown that rat cortical (external capsule) afferents express postsynaptic alterations during chronic intermittent ethanol exposure and withdrawal. However, thalamic (internal capsule) afferents also provide crucial glutamatergic input during behavioral conditioning, and they have not been studied in the context of chronic drug exposure. We report here that these thalamic inputs express altered presynaptic function during withdrawal from chronic ethanol exposure. This is characterized by enhanced release probability, as exemplified by altered paired-pulse ratios and decreased failure rates of unitary events, and increased concentrations of synaptic glutamate. Quantal analysis further implicates a withdrawal-dependent enhancement of the readily releasable pool of vesicles as a probable mechanism. These functional alterations are accompanied by increased expression of vesicle associated protein markers. These data demonstrate that chronic ethanol modulation of glutamate neurotransmission in the rat lateral/basolateral amygdala is afferent-specific. Further, presynaptic regulation of lateral/basolateral amygdala thalamic inputs by chronic ethanol may be a novel neurobiological mechanism contributing to the increased anxiety-like behaviors that characterize withdrawal.

Indexed as

Afferent PathwaysAmygdalaAnimalsEthanolExcitatory Postsynaptic PotentialsGlutamic AcidMaleOrgan Culture TechniquesPresynaptic TerminalsRatsRats, Sprague-DawleySubstance Withdrawal SyndromeThalamusEthanolGlutamic Acid

Identifiers

PMID22982568
PMCPMC3521082
OpenAlexW2071727739

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.