Evidence map›Paper›PMID 21447066›Full record

ArticleJournal of neuroendocrinology2011

Brain stem catecholamines circuitry: activation by alcohol and role in the hypothalamic-pituitary-adrenal response to this drug.

S Lee, Z Craddock, C Rivier

Abstract read
In one paragraph

Article in Journal of neuroendocrinology, 2011. 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 33% 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, 30 citations in OpenAlex.

  1. Sex differences in neural circuits driving binge-like drinking: a female-specific role for an amygdalo-striatal pathway.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Article
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  5. Validity of mental and physical stress models.Neuroscience and biobehavioral reviews · 2024
    Review
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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

3 authors at 1 institution in 1 country.

S LeeThe Clayton Foundation Laboratories for Peptide Biology, The Salk Institute, La Jolla, CA, USA.
Z Craddock
C Rivier
Salk Institute for Biological Studies · US

Funding

Viral Vector CoreP60AA006420 · NIAAA · SCRIPPS RESEARCH INSTITUTE, THE · PI ERIC P ZORRILLA · 2003 to 2026
$46.3M
ALCOHOL INTERLEUKIN INTERACTIONS on the HPA AxisR37AA008924 · NIAAA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI RIVIER, CATHERINE L · 2000 to 2009
$5.5M
SYSTEMIC NEUROPHARMACOLOGYP50AA006420 · NIAAA · SCRIPPS RESEARCH INSTITUTE · PI KOOB, GEORGE F · 1985 to 2002
$5.1M
ALCOHOL/INTERLEUKIN INTERACTIONS ON THE RAT HPA AXISR01AA008924 · NIAAA · SALK INSTITUTE FOR BIOLOGICAL STUDIES · PI RIVIER, CATHERINE L · 1991 to 1999
–
NIAAA NIH HHS AA006420NIAAA NIH HHS AA008924NIAAA NIH HHS P50 AA006420NIAAA NIH HHS P60 AA006420NIAAA NIH HHS R01 AA008924NIAAA NIH HHS R37 AA008924
6 · The paper itself

Abstract

Although the stimulatory effect of alcohol on the rat hypothalamic-pituitary-adrenal (HPA) axis is well known, the mechanisms underlying this influence remain poorly understood. In the present study, we tested the hypothesis that brain catecholamines play an important role in this response. As expected, the acute intragastric administration of alcohol to adult male rats elevated plasma adrenocorticotrophic hormone (ACTH) levels and activated hypothalamic corticotrophin-releasing factor neurones. Novel findings pertain to the effect of alcohol on, and the role played by, brain adrenergic circuits. We first observed that alcohol up-regulated c-fos signals in the locus coeruleus, the main noradrenergic brain cell group; and that it activated (nor)adrenergic medullary cells (A1-A2/C1-C3). Evidence for the role played by these catecholaminergic circuits then came from the observation that blockade of α(1) -, but not β-, adrenergic receptors interfered with alcohol-induced ACTH secretion; and that depletion of catecholaminergic input to the paraventricular nucleus (PVN) by the toxin 6-hydroxydopamine significantly decreased the ACTH response to alcohol. Finally, destruction of the A1-A2/C1-C3 region with the immunotoxin anti-dopamine-B-hydroxylase-saporin interfered with the catecholaminergic input to the PVN. Collectively, our work extends our knowledge of the ability of this drug to up-regulate catecholamine circuitry in the rat brain. It also shows that medullary catecholamine innervation of the hypothalamus plays an important role in modulating the stimulatory effect of alcohol on the HPA axis, an effect exerted through activation of α(1) -adrenergic receptors.

Indexed as

AmygdalaAnimalsBrain StemCatecholaminesEthanolHypothalamo-Hypophyseal SystemHypothalamusMaleNerve NetNorepinephrineParaventricular Hypothalamic NucleusPituitary-Adrenal SystemRatsRats, Sprague-DawleyReceptors, AdrenergicCatecholaminesEthanolNorepinephrineReceptors, Adrenergic

Identifiers

PMID21447066
PMCPMC3176674
OpenAlexW1546738173

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.