Evidence map›Paper›PMID 28036359›Full record

ArticlePloS one2016

Transient Activation of GABAB Receptors Suppresses SK Channel Currents in Substantia Nigra Pars Compacta Dopaminergic Neurons.

Chad M Estep, Daniel J Galtieri, Enrico Zampese, Joshua A Goldberg, Lars Brichta, Paul Greengard, D James Surmeier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 34% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. Activation of GABAJournal of neurophysiology · 2020
    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

7 authors at 3 institutions in 2 countries.

Chad M EstepDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States of America.
Daniel J GaltieriDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States of America.
Enrico ZampeseDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States of America.
Joshua A GoldbergDepartment of Medical Neurobiology, Institute of Medical Research Israel-Canada, Faculty of Medicine, The Hebrew University of Jerusalem, Jerusalem, Israel.
Lars BrichtaLaboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY, United States of America.
Paul GreengardLaboratory of Molecular and Cellular Neuroscience, Rockefeller University, New York, NY, United States of America.
D James SurmeierDepartment of Physiology, Feinberg School of Medicine, Northwestern University, Chicago, IL, United States of America.
Northwestern University · USRockefeller University · USHebrew University of Jerusalem · IL

Funding

SYNAPTIC CONTROLOF PALLIDAL ACTIVITYP50NS047085 · NINDS · NORTHWESTERN UNIVERSITY AT CHICAGO · PI SURMEIER, DALTON JAMES · 2003 to 2018
$19.2M
NINDS NIH HHS P50 NS047085
6 · The paper itself

Abstract

Dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc) are richly innervated by GABAergic neurons. The postsynaptic effects of GABA on SNc DA neurons are mediated by a mixture of GABAA and GABAB receptors. Although activation of GABAA receptors inhibits spike generation, the consequences of GABAB receptor activation are less well characterized. To help fill this gap, perforated patch recordings were made from young adult mouse SNc DA neurons. Sustained stimulation of GABAB receptors hyperpolarized SNc DA neurons, as previously described. However, transient stimulation of GABAB receptors by optical uncaging of GABA did not; rather, it reduced the opening of small-conductance, calcium-activated K+ (SK) channels and increased the irregularity of spiking. This modulation was attributable to inhibition of adenylyl cyclase and protein kinase A. Thus, because suppression of SK channel activity increases the probability of burst spiking, transient co-activation of GABAA and GABAB receptors could promote a pause-burst pattern of spiking.

Indexed as

Adenylyl CyclasesAnimalsCyclic AMP-Dependent Protein KinasesDopaminergic NeuronsFemaleGABAergic Neuronsgamma-Aminobutyric AcidIon Channel GatingMaleMiceMice, Inbred C57BLPars CompactaPatch-Clamp TechniquesReceptors, GABA-AReceptors, GABA-BSmall-Conductance Calcium-Activated Potassium ChannelsAdenylyl CyclasesCyclic AMP-Dependent Protein Kinasesgamma-Aminobutyric AcidReceptors, GABA-AReceptors, GABA-BSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID28036359
PMCPMC5201262
OpenAlexW2570371570

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.