Evidence map›Paper›PMID 12097489›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

Somatostatin inhibits thalamic network oscillations in vitro: actions on the GABAergic neurons of the reticular nucleus.

Qian-Quan Sun, John R Huguenard, David A Prince

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

28 citing papers in PubMed, 70 citations in OpenAlex.

  1. Neuropeptidergic systems in psychiatric disorders.Frontiers in endocrinology · 2025
    Review
  2. Article
  3. Cell-Type-Specific Effects of Somatostatin on Synaptic Transmission in the Anterior Cingulate Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  4. Review
  5. Neuronal G protein-gated KAmerican journal of physiology. Cell physiology · 2022
    Review
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  7. Article
  8. Article
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  11. 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

3 authors at 2 institutions in 1 country.

Qian-Quan SunDepartment of Neurology and Neurological Science, Stanford School of Medicine, Stanford, California 94305, USA.
John R Huguenard
David A Prince
Stanford Medicine · USStanford University · US

Funding

REGULATION OF NEURONAL EXCITABILITY IN CHRONIC EPILEPTOGENESISP50NS012151 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1985 to 2007
$9.1M
Epilepsy Research ProgramP01NS012151 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 2008 to 2011
$4.4M
NINDS NIH HHS NS12151NINDS NIH HHS P01 NS012151NINDS NIH HHS P50 NS012151
6 · The paper itself

Abstract

We examined the effects of somatostatin (SST) on neurons in the thalamic reticular nucleus (RT) using whole-cell patch-clamp techniques applied to visualized neurons in rat thalamic slices. SST, acting via sst(5) receptors and pertussis toxin-sensitive G-proteins, activated an inwardly rectifying K(+) (GIRK) current in 20 of 28 recorded cells to increase input conductance 15 +/- 3% above control and inhibited N-type Ca(2+) currents in 17 of 24 neurons via voltage-dependent mechanisms. SST reversibly depressed evoked EPSCs (eEPSCs) to 37 +/- 8% of control without altering their kinetics. SST-mediated inhibition of eEPSCs showed short-term relief from block during 25 Hz stimulus trains. SST also reduced the frequency (33 +/- 8%) but not the amplitude of miniature EPSCs (mEPSCs). These data indicate that SST mediates presynaptic inhibition of glutamate release onto RT neurons. In current-clamp recordings, SST preferentially inhibited burst discharges mediated by near-threshold corticothalamic EPSPs and intracellularly applied depolarizing currents. SST had powerful effects on in vitro intrathalamic rhythms, which included a shortening of the duration and a reduction in spike count within each oscillatory event. Furthermore, there was a paradoxical increase in the synchrony of epileptiform oscillations, likely mediated by a suppression of the responses to weak synaptic inputs in RT. We conclude that SST suppresses discharges in RT neurons, via presynaptic inhibition of glutamate release and postsynaptic activation of GIRK channels, leading to the dampening of both spindle-like and epileptiform thalamic network oscillations. SST may act as an important endogenous regulator of physiological and pathological thalamocortical network activities.

Indexed as

AnimalsCalcium Channel BlockersCalcium ChannelsCulture TechniquesElectric ConductivityEvoked Potentialsgamma-Aminobutyric AcidHeterotrimeric GTP-Binding ProteinsNeuronsPeriodicityPotassium Channel BlockersPotassium Channels, Inwardly RectifyingPresynaptic TerminalsRatsRats, Sprague-DawleyReceptors, SomatostatinCalcium Channel BlockersCalcium Channelsgamma-Aminobutyric AcidHeterotrimeric GTP-Binding ProteinsPotassium Channel BlockersPotassium Channels, Inwardly RectifyingReceptors, SomatostatinSomatostatinsomatostatin receptor 5

Identifiers

PMID12097489
PMCPMC6758225
OpenAlexW2169221312

What OpenQuestion holds

Textmetadata
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.