Evidence map›Paper›PMID 26707595›Full record

ArticleNeuropharmacology2016

Acute and chronic ethanol exposure differentially regulate CB1 receptor function at glutamatergic synapses in the rat basolateral amygdala.

Stacey L Robinson, Nancy J Alexander, Rebecca J Bluett, Sachin Patel, Brian A McCool

Abstract read
In one paragraph

Article in Neuropharmacology, 2016. 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
3.1field-weighted citation impact, top 9% 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, 27 citations in OpenAlex.

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  6. Intoxicating effects of alcohol depend on acid-sensing ion channels.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
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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

5 authors at 2 institutions in 1 country.

Stacey L RobinsonDepartment of Physiology & Pharmacology, Winston-Salem NC, USA; Neuroscience and Alcohol Research Training Programs Wake Forest School Medicine, Winston-Salem NC, USA.
Nancy J AlexanderDepartment of Physiology & Pharmacology, Winston-Salem NC, USA.
Rebecca J BluettDepartment of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN, USA.
Sachin PatelDepartment of Psychiatry, Vanderbilt University School of Medicine, Nashville, TN, USA; Vanderbilt Brain Institute, Vanderbilt University School of Medicine, Nashville, TN, USA; Vanderbilt-Kennedy Center for Research on Human Development, Vanderbilt University School of Medicine, Nashville, TN, USA; Department Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, TN, USA.
Brian A McCoolDepartment of Physiology & Pharmacology, Winston-Salem NC, USA; Neuroscience and Alcohol Research Training Programs Wake Forest School Medicine, Winston-Salem NC, USA. Electronic address: bmccool@wakehealth.edu.
Vanderbilt University · USWake 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
Research Project: Sensory and Multisensory Contributions to AutismU54HD083211 · NICHD · VANDERBILT UNIVERSITY MEDICAL CENTER · PI CUTTING, LAURIE E · 2015 to 2019
$7.1M
The Ethanol - Anxiety Interaction: Cellular MechanismsR01AA014445 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCOOL, BRIAN A · 2004 to 2023
$5.2M
Translational Studies on Early-life Stress and Vulnerability to Alcohol AddictionP01AA021099 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI JONES, SARA RAULERSON · 2012 to 2016
$2.8M
Substrate-selective inhibition of COX-2 to target affective disordersR01MH100096 · NIMH · VANDERBILT UNIVERSITY MEDICAL CENTER · PI PATEL, SACHIN · 2013 to 2018
$2.4M
Ethanol Dependence Induced Changes in Dopamine Signaling in Basolateral AmygdalaR01AA023999 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI JONES, SARA RAULERSON, MCCOOL, BRIAN A · 2015 to 2019
$1.8M
Withdrawal-Stress, Anxiety, and Amygdala NeurophysiologyU01AA020942 · NIAAA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MCCOOL, BRIAN A · 2012 to 2016
$911k
Afferent-specific Endocannabinoid Signaling in the Central AmygdalaR21MH103515 · NIMH · VANDERBILT UNIVERSITY · PI PATEL, SACHIN · 2014 to 2015
$412k
2-Arachidonoylglycerol Signaling Relieves Stress-induced AnxietyF31MH106192 · NIMH · VANDERBILT UNIVERSITY · PI BLUETT, REBECCA J · 2015 to 2017
$90k
NIAAA NIH HHS P01 AA021099NIAAA NIH HHS R01 AA014445NIAAA NIH HHS R01 AA023999NIAAA NIH HHS T32 AA007565NIAAA NIH HHS U01 AA020942NICHD NIH HHS U54 HD083211NIMH NIH HHS F31 MH106192NIMH NIH HHS R01 MH100096NIMH NIH HHS R21 MH103515
6 · The paper itself

Abstract

The endogenous cannabinoid (eCB) system has been suggested to play a key role in ethanol preference and intake, the acute effects of ethanol, and in the development of withdrawal symptoms following ethanol dependence. Ethanol-dependent alterations in glutamatergic signaling within the lateral/basolateral nucleus of the amygdala (BLA) are critical for the development and expression of withdrawal-induced anxiety. Notably, the eCB system significantly regulates both glutamatergic and GABAergic synaptic activity within the BLA. Chronic ethanol exposure significantly alters eCB system expression within regions critical to the expression of emotionality and anxiety-related behavior, including the BLA. Here, we investigated specific interactions between the BLA eCB system and its functional regulation of synaptic activity during acute and chronic ethanol exposure. In tissue from ethanol naïve-rats, a prolonged acute ethanol exposure caused a dose dependent inhibition of glutamatergic synaptic activity via a presynaptic mechanism that was occluded by CB1 antagonist/inverse agonists SR141716a and AM251. Importantly, this acute ethanol inhibition was attenuated following 10 day chronic intermittent ethanol vapor exposure (CIE). CIE exposure also significantly down-regulated CB1-mediated presynaptic inhibition at glutamatergic afferent terminals but spared CB1-inhibition of GABAergic synapses arising from local inhibitory-interneurons. CIE also significantly elevated BLA N-arachidonoylethanolamine (AEA or anandamide) levels and decreased CB1 receptor protein levels. Collectively, these data suggest a dynamic regulation of the BLA eCB system by acute and chronic ethanol.

Indexed as

AnimalsBasolateral Nuclear ComplexDose-Response Relationship, DrugDrug Administration ScheduleEthanolExcitatory Postsynaptic PotentialsGlutamic AcidMaleOrgan Culture TechniquesRatsRats, Sprague-DawleyReceptor, Cannabinoid, CB1SynapsesEthanolGlutamic AcidReceptor, Cannabinoid, CB1AnandamideBasolateral amygdalaCB1DependenceEndogenous cannabinoidEthanol

Identifiers

PMID26707595
PMCPMC4912876
OpenAlexW2211514088

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.