Evidence map›Paper›PMID 35915568›Full record

ArticleAlcoholism, clinical and experimental research2022

The ethanol inhibition of basolateral amygdala neuron spiking is mediated by a γ-aminobutyric acid type A-mediated tonic current.

Sudarat Nimitvilai-Roberts, John J Woodward

Open access · greenAbstract read
In one paragraph

Article in Alcoholism, clinical and experimental research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 62% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Article
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.

Sudarat Nimitvilai-RobertsDepartment of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA.
John J WoodwardDepartment of Neuroscience, Medical University of South Carolina, Charleston, South Carolina, USA.ORCID 0000-0003-2382-4005
Medical University of South Carolina · US

Funding

TREATING ETHANOL WITHDRAWAL WITH LORAZEPAM/NALTREXONEP50AA010761 · NIAAA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI HOWARD C. BECKER · 1996 to 2026
$46.8M
NIAAA NIH HHS P50 AA010761
6 · The paper itself

Abstract

backgroundThe basolateral nucleus of the amygdala (BLA) plays an important role in the development of fear and anxiety-related behaviors. The BLA receives inputs from all sensory stimuli. After processing those stimuli, BLA neurons signal neurons within the central amygdala and other brain regions, including the ventral and dorsal striatum and frontal cortex. Studies suggest that the BLA is involved in drug dependence and in the reinforcing actions of ethanol. For example, acute exposure to ethanol reduces anxiety, while withdrawal from chronic ethanol exposure alters BLA synaptic transmission, which increases anxiety, a common underlying cause of relapse. Exposure to and withdrawal from chronic alcohol also disrupts many brain areas that connect with the BLA. Despite these important findings, the acute actions of alcohol on the intrinsic excitability of BLA neurons have not been fully characterized.

methodsBrain slices containing the BLA were prepared from adult C57BL/6J male mice. Whole-cell and sharp electrode electrophysiological recordings were performed to characterize the effects of acute ethanol on BLA neuronal and astrocyte function, respectively.

resultsEthanol inhibited action potential (AP) firing of BLA neurons but had no effect on BLA astrocyte resting membrane potential. The ethanol-induced inhibition of firing was concentration-dependent (11 to 66 mM) and accompanied by a reduction in the input resistance and an increase in the rheobase of BLA neurons. The inhibitory effect of ethanol was suppressed by picrotoxin, which blocks both γ-aminobutyric acid type A (GABA

conclusionsThese results suggest that BLA neurons express a GABA-mediated tonic current that is enhanced by acute ethanol, which leads to reduced excitability of BLA neurons.

Indexed as

Basolateral Nuclear ComplexCentral Amygdaloid NucleusAnimalsEthanolgamma-Aminobutyric AcidMaleMiceMice, Inbred C57BLNeuronsPicrotoxinReceptors, GABA-AReceptors, GlycineStrychnineSynaptic TransmissionEthanolgamma-Aminobutyric AcidPicrotoxinReceptors, GABA-AReceptors, GlycineStrychninebasolateral amygdalaethanolGABAA-mediated tonic currentsintrinsic excitability

Identifiers

PMID35915568
PMCPMC9509443
OpenAlexW4289526377

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.