Evidence map›Paper›PMID 16990402›Full record

ArticleThe Journal of physiology2006

Thyrotropin-releasing hormone increases GABA release in rat hippocampus.

Pan-Yue Deng, James E Porter, Hee-Sup Shin, Saobo Lei

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 67 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Biochemical and physiological insights into TRH receptor-mediated signaling.Frontiers in cell and developmental biology · 2022
    Review
  5. Article
  6. Review
  7. Roles of KNeuropharmacology · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. fosB-null mice display impaired adult hippocampal neurogenesis and spontaneous epilepsy with depressive behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013
    Article
  19. Article
  20. The role of Thyrotropin Releasing Hormone in aging and neurodegenerative diseases.American journal of Alzheimer's disease (Columbia, Mo.) · 2013
    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

4 authors at 2 institutions in 2 countries.

Pan-Yue DengDepartment of Pharmacology, Physiology and Therapeutics, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203, USA.
James E Porter
Hee-Sup Shin
Saobo Lei
University of North Dakota · USKorea Institute of Science and Technology · KR

Funding

TRPC1, CALCIUM AND PARKINSON'S DISEASEP20RR017699 · NCRR · UNIVERSITY OF NORTH DAKOTA · PI GHRIBI, OTHMAN · 2002 to 2011
$19.7M
NCRR NIH HHS 5P20RR017699-02NCRR NIH HHS P20 RR017699
6 · The paper itself

Abstract

Thyrotropin-releasing hormone (TRH) is a tripeptide that is widely distributed in the brain including the hippocampus where TRH receptors are also expressed. TRH has anti-epileptic effects and regulates arousal, sleep, cognition, locomotion and mood. However, the cellular mechanisms underlying such effects remain to be determined. We examined the effects of TRH on GABAergic transmission in the hippocampus and found that TRH increased the frequency of GABAA receptor-mediated spontaneous IPSCs in each region of the hippocampus but had no effects on miniature IPSCs or evoked IPSCs. TRH increased the action potential firing frequency recorded from GABAergic interneurons in CA1 stratum radiatum and induced membrane depolarization suggesting that TRH increases the excitability of interneurons to facilitate GABA release. TRH-induced inward current had a reversal potential close to the K+ reversal potential suggesting that TRH inhibits resting K+ channels. The involved K+ channels were sensitive to Ba2+ but resistant to other classical K+ channel blockers, suggesting that TRH inhibits the two-pore domain K+ channels. Because the effects of TRH were mediated via Galphaq/11, but were independent of its known downstream effectors, a direct coupling may exist between Galphaq/11 and K+ channels. Inhibition of the function of dynamin slowed the desensitization of TRH responses. TRH inhibited seizure activity induced by Mg2+ deprivation, but not that generated by picrotoxin, suggesting that TRH-mediated increase in GABA release contributes to its anti-epileptic effects. Our results demonstrate a novel mechanism to explain some of the hippocampal actions of TRH.

Indexed as

Action PotentialsAnimalsAnticonvulsantsDynaminsgamma-Aminobutyric AcidGTP-Binding Protein alpha Subunits, Gq-G11HippocampusInhibitory Postsynaptic PotentialsInterneuronsIn Vitro TechniquesIsoenzymesMiceMice, Inbred C57BLMice, TransgenicNeural InhibitionPatch-Clamp TechniquesAnticonvulsantsDynaminsgamma-Aminobutyric AcidGTP-Binding Protein alpha Subunits, Gq-G11IsoenzymesPhospholipase C betaPotassiumPotassium Channels, Tandem Pore DomainReceptors, GABA-AThyrotropin-Releasing HormoneType C Phospholipases

Identifiers

PMID16990402
PMCPMC1890442
OpenAlexW1486689401

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.