Evidence map›Paper›PMID 21624785›Full record

ArticleAlcohol (Fayetteville, N.Y.)2011

Acute ethanol exposure prevents PMA-mediated augmentation of N-methyl-D-aspartate receptor function in primary cultured cerebellar granule cells.

Jason Reneau, Mary E Reyland, R Lisa Popp

Abstract read
In one paragraph

Article in Alcohol (Fayetteville, N.Y.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.7field-weighted citation impact, top 37% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Ethanol Reversal of Tolerance to the Respiratory Depressant Effects of Morphine.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Article
  5. Article
  6. Article
  7. 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

3 authors at 2 institutions in 1 country.

Jason ReneauDepartment of Pharmacology and Neuroscience, Texas Tech University Health Sciences Center, Lubbock, 79430-0002, USA.
Mary E Reyland
R Lisa Popp
Texas Tech University Health Sciences Center · USUniversity of Colorado Denver · US

Funding

Regulation of Salivary Cell Apoptosis by Protein Kinase CR01DE015648 · NIDCR · UNIVERSITY OF COLORADO DENVER · PI REYLAND, MARY ELAINE · 2004 to 2019
$5.6M
Protein Kinase C Modulation of NMDAR Ethanol SensitivityR01AA013436 · NIAAA · UNIVERSITY OF TEXAS AUSTIN · PI POPP, ROSEANNA LISA · 2002 to 2006
$1.1M
NIAAA NIH HHS R01 AA013436NIAAA NIH HHS R01AA13436NIDCR NIH HHS R01 DE015648NIDCR NIH HHS R01DE015648
6 · The paper itself

Abstract

Many intracellular proteins and signaling cascades contribute to the ethanol sensitivity of native N-methyl-D-aspartate receptors (NMDARs). One putative protein is the serine/threonine kinase, protein kinase C (PKC). The purpose of this study was to assess if PKC modulates the ethanol sensitivity of native NMDARs expressed in primary cultured cerebellar granule cells (CGCs). With the whole-cell patch-clamp technique, we assessed if ethanol inhibition of NMDA-induced currents (I(NMDA)) (100 μM NMDA plus 10 μM glycine) were altered in CGCs in which the novel and classical PKC isoforms were activated by phorbol-12-myristate-13-acetate (PMA). Percent inhibition by 10, 50, or 100 mM ethanol of NMDA-induced steady-state current amplitudes (I(SS)) or peak current amplitudes (I(Pk)) of NMDARs expressed in CGCs in which PKC was activated by a 12.5 min, 100 nM PMA exposure at 37°C did not differ from currents obtained from receptors contained in control cells. However, PMA-mediated augmentation of I(Pk) in the absence of ethanol was abolished after brief applications of 10 or 1 mM ethanol coapplied with agonists, and this suppression of enhanced receptor function was observed for up to 8 min post-ethanol exposure. Because we had previously shown that PMA-mediated augmentation of I(NMDA) of NMDARs expressed in these cells is by activation of PKCα, we assessed the effect of ethanol (1, 10, 50, and 100 mM) on PKCα activity. Ethanol decreased PKCα activity by 18% for 1 mM ethanol and activity decreased with increasing ethanol concentrations with a 50% inhibition observed with 100 mM ethanol. The data suggest that ethanol disruption of PMA-mediated augmentation of I(NMDA) may be due to a decrease in PKCα activity by ethanol. However, given the incomplete blockade of PKCα activity and the low concentration of ethanol at which this phenomenon is observed, other ethanol-sensitive signaling cascades must also be involved.

Indexed as

AnimalsCells, CulturedCerebellumEthanolPatch-Clamp TechniquesProtein Kinase C-alphaRatsRats, Sprague-DawleyReceptors, N-Methyl-D-AspartateTetradecanoylphorbol AcetateEthanolProtein Kinase C-alphaReceptors, N-Methyl-D-AspartateTetradecanoylphorbol Acetate

Identifiers

PMID21624785
PMCPMC3154614
OpenAlexW2022111436

What OpenQuestion holds

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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.