Evidence map›Paper›PMID 39827996›Full record

ArticleNeuropharmacology2025

Age- and cytokine-dependent modulation of GABAergic transmission within the basolateral amygdala of male Sprague Dawley rats.

Marvin R Diaz, Thaddeus M Barney, Paige Marsland, Terrence Deak

Abstract read
In one paragraph

Article in Neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. 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.

Marvin R DiazDevelopmental Exposure Alcohol Research Center, Behavioral Neuroscience Program, Department of Psychology, Binghamton, NY, 13902-6000, USA.
Thaddeus M BarneyDevelopmental Exposure Alcohol Research Center, Behavioral Neuroscience Program, Department of Psychology, Binghamton, NY, 13902-6000, USA.
Paige MarslandDevelopmental Exposure Alcohol Research Center, Behavioral Neuroscience Program, Department of Psychology, Binghamton, NY, 13902-6000, USA.
Terrence DeakDevelopmental Exposure Alcohol Research Center, Behavioral Neuroscience Program, Department of Psychology, Binghamton, NY, 13902-6000, USA. Electronic address: tdeak@binghamton.edu.

Funding

Social Anxiety, Stress and Ethanol Sensitivity in Adolescence and AdulthoodP50AA017823 · NIAAA · UPSTATE MEDICAL UNIVERSITY · PI J. DAVID JENTSCH · 2009 to 2026
$30.5M
Development and Neuroadaptations in Alcohol and Addictions (DNA2)T32AA025606 · NIAAA · STATE UNIVERSITY OF NY,BINGHAMTON · PI J. DAVID JENTSCH · 2017 to 2026
$2.7M
NIAAA NIH HHS P50 AA017823NIAAA NIH HHS T32 AA025606
6 · The paper itself

Abstract

Alcohol binge drinking has a multitude of effects on CNS function, including changes in inflammatory cytokines such as IL-6 and IL-1β that may contribute to mood fluctuations associated with the intoxication-withdrawal cycle. Widely throughout the brain, including the amygdala, IL-6 mRNA is enhanced during intoxication, whereas IL-1β is initially suppressed during alcohol intoxication, with increased expression seen shortly after ethanol clearance, during acute hangover. Furthermore, induction of neuroimmune genes appears to be muted during adolescence in the amygdala, suggesting a broader functional immaturity of the adolescent neuroimmune system in structures involved in negative affect associated with ethanol exposure. However, neither the effect of IL-6 or IL-1β on synaptic function within the amygdala nor the impact of acute intoxication and withdrawal on these cytokines' function are known. To test this, we used whole-cell patch-clamp electrophysiology to assess the effects of IL-6 and IL-1β on GABA-mediated spontaneous inhibitory postsynaptic currents (sIPSCs) in BLA pyramidal neurons from male rats in early adolescence (P28-40) or adulthood (P70+). These experiments were done in naïve, intoxicated (3-4 h following an intraperitoneal injection of 3.5 g/kg ethanol), and during acute hangover (11-18 h post ethanol injection). In naïve males, we found that IL-6 (10 ng/ml) significantly enhanced sIPSC amplitude only in adults, with no apparent effect in adolescents; this effect of IL-6 in adults was not different during intoxication. Conversely, IL-1β (10 ng/ml) did not alter sIPSC frequency in any group (naïve or hangover adolescents or adults). Unlike our previous work in adult rats, here we found that contextual fear conditioning was not altered in adolescents when conditioned during acute hangover. Together, these observations suggest that IL-6, but not IL-1β, regulation of BLA GABA transmission emerges as a function of age, but is not affected by acute ethanol exposure or hangover for adolescents or adults. Importantly, these findings provide additional evidence to support functional immaturity of the neuroimmune system in adolescence.

Indexed as

Basolateral Nuclear Complexgamma-Aminobutyric AcidInterleukin-1betaInterleukin-6Synaptic TransmissionAge FactorsAnimalsEthanolInhibitory Postsynaptic PotentialsMalePatch-Clamp TechniquesPyramidal CellsRatsRats, Sprague-DawleyEthanolgamma-Aminobutyric AcidInterleukin-1betaInterleukin-6AcuteAdolescenceAlcoholCytokineDevelopmentHangoverNeuroimmuneWithdrawal

Identifiers

PMID39827996
PMCPMC12359078

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Registered trials

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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.