Evidence map›Paper›PMID 19171770›Full record

ArticleThe Journal of general physiology2009

Pentobarbital produces activation and block of {alpha}1{beta}2{gamma}2S GABAA receptors in rapidly perfused whole cells and membrane patches: divergent results can be explained by pharmacokinetics.

Kevin J Gingrich, Paul M Burkat, William A Roberts

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of general physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
0.6field-weighted citation impact, top 36% 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

15 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Review
  3. GABAFrontiers in cellular neuroscience · 2020
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. High membrane permeability for melatonin.The Journal of general physiology · 2016
    Article
  9. Article
  10. Article
  11. α1F64 Residue at GABA(A) receptor binding site is involved in gating by influencing the receptor flipping transitions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  12. Article
  13. Article
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  15. 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 1 institution in 1 country.

Kevin J GingrichDepartment of Anesthesiology, New York University Langone Medical Center, New York, NY 10016, USA. kevin.gingrich@med.nyu.edu
Paul M Burkat
William A Roberts
University of Rochester · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Millimolar concentrations of the barbiturate pentobarbital (PB) activate gamma-aminobutyric acid (GABA) type A receptors (GABARs) and cause blockade reported by a paradoxical current increase or "tail" upon washout. To explore the mechanism of blockade, we investigated PB-triggered currents of recombinant alpha(1)beta(2)gamma(2S) GABARs in whole cells and outside-out membrane patches using rapid perfusion. Whole cell currents showed characteristic bell-shaped concentration dependence where high concentrations triggered tail currents with peak amplitudes similar to those during PB application. Tail current time courses could not be described by multi-exponential functions at high concentrations (> or =3,000 microM). Deactivation time course decayed over seconds and was slowed by increasing PB concentration and application time. In contrast, macropatch tail currents manifested eightfold greater relative amplitude, were described by multi-exponential functions, and had millisecond rise times; deactivation occurred over fractions of seconds and was insensitive to PB concentration and application time. A parsimonious gating model was constructed that accounts for macropatch results ("patch" model). Lipophilic drug molecules migrate slowly through cells due to avid partitioning into lipophilic subcellular compartments. Inclusion of such a pharmacokinetic compartment into the patch model introduced a slow kinetic component in the extracellular exchange time course, thereby providing recapitulation of divergent whole cell results. GABA co-application potentiated PB blockade. Overall, the results indicate that block is produced by PB concentrations sixfold lower than for activation involving at least three inhibitory PB binding sites, suggest a role of blocked channels in GABA-triggered activity at therapeutic PB concentrations, and raise an important technical question regarding the effective rate of exchange during rapid perfusion of whole cells with PB.

Indexed as

AnimalsBinding SitesCell CompartmentationDose-Response Relationship, DrugFeedback, PhysiologicalGABA-A Receptor AgonistsGABA-A Receptor AntagonistsGABA Modulatorsgamma-Aminobutyric AcidHumansIntracellular SpaceIon Channel GatingIon TransportModels, BiologicalPatch-Clamp TechniquesPentobarbitalGABA-A Receptor AgonistsGABA-A Receptor AntagonistsGABA Modulatorsgamma-Aminobutyric AcidPentobarbitalProtein SubunitsReceptors, GABA-A

Identifiers

PMID19171770
PMCPMC2638204
OpenAlexW2171445221

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.