Evidence map›Paper›PMID 19963045›Full record

ArticleNeuroscience2010

Presynaptic 5-HT(1B) receptor-mediated serotonergic inhibition of glutamate transmission in the bed nucleus of the stria terminalis.

J-D Guo, D G Rainnie

Abstract read
In one paragraph

Article in Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.8field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 66 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. The 5-HTPsychopharmacology · 2018
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Stress Modulation of Opposing Circuits in the Bed Nucleus of the Stria Terminalis.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016
    Review
  14. Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

J-D GuoDepartment of Psychiatry and Behavioral Sciences, Yerkes National Primate Research Center, Emory University, Atlanta, GA, USA.
D G Rainnie
Emory University · US

Funding

YNPRC NHP CLINICAL MEDICINE RESIDENCY PROGRAM - SUPPLEMENTP51RR000165 · NCRR · EMORY UNIVERSITY · PI ALTMAN, JOHN DAVID · 1985 to 2011
$114.0M
Stress-Induced Gene Regulation: BNST CRF Neurons and the Physiology of AnxietyR01MH072908 · NIMH · EMORY UNIVERSITY · PI YOUNG, LARRY J · 2005 to 2020
$6.0M
NCRR NIH HHS P51 RR000165NCRR NIH HHS RR-00165NIMH NIH HHS MH072908NIMH NIH HHS R01 MH072908
6 · The paper itself

Abstract

Activation of neurons in the bed nucleus of the stria terminalis (BNST) plays a critical role in stress and anxiety-related behaviors. Previously, we have shown that serotonin (5-HT) can directly modulate BNST neuronal excitability by an action at postsynaptic receptors. In this study we built upon that work to examine the effects of 5-HT on excitatory neurotransmission in an in vitro rat BNST slice preparation. Bath application of 5-HT reversibly reduced the amplitude of evoked excitatory postsynaptic currents (eEPSCs). These effects were mimicked by the 5-HT(1B/D) receptor agonist, sumatriptan, and by the 5-HT(1B) receptor selective agonist, CP93129. Conversely, the effects of 5-HT and sumatriptan could be blocked by the 5-HT(1B) receptor-selective antagonist, GR55562. In contrast, the 5-HT(1A) receptor agonist 8-OH DPAT or antagonist WAY 100635 could not mimic or block the effect of 5-HT on eEPSCs. Together, these data suggest that the 5-HT-induced attenuation of eEPSCs was mediated by 5-HT(1B) receptor activation. Moreover, sumatriptan had no effect on the amplitude of the postsynaptic current elicited by pressure applied AMPA, suggesting a possible presynaptic locus for the 5-HT(1B) receptor. Furthermore, 5-HT, sumatriptan and CP93129 all increased the paired pulse ratio of eEPSCs while they concomitantly decreased the amplitude of eEPSCs, suggesting that these agonists act to reduce glutamate release probability at presynaptic locus. Consistent with this observation, sumatriptan decreased the frequency of miniature EPSCs, but had no effect on their amplitude. Taken together, these results suggest that 5-HT suppresses glutamatergic neurotransmission in the BNST by activating presynaptic 5-HT(1B) receptors to decrease glutamate release from presynaptic terminals. This study illustrates a new pathway by which the activity of BNST neurons can be indirectly modulated by 5-HT, and suggests a potential new target for the development of novel treatments for depression and anxiety disorders.

Indexed as

alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidAnimalsEvoked PotentialsExcitatory Postsynaptic PotentialsGlutamic AcidIn Vitro TechniquesMaleMembrane PotentialsNeural InhibitionNeuronsPresynaptic TerminalsRatsRats, Sprague-DawleyReceptor, Serotonin, 5-HT1AReceptor, Serotonin, 5-HT1BReceptor, Serotonin, 5-HT1Dalpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic AcidGlutamic AcidReceptor, Serotonin, 5-HT1AReceptor, Serotonin, 5-HT1BReceptor, Serotonin, 5-HT1DSerotoninSerotonin 5-HT1 Receptor AgonistsSerotonin 5-HT1 Receptor Antagonists

Identifiers

PMID19963045
PMCPMC2815192
OpenAlexW2093673274

What OpenQuestion holds

Textmetadata
LicenceTDM
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.