Evidence map›Paper›PMID 22884625›Full record

ArticleNeuropharmacology2012

Vasopressin facilitates GABAergic transmission in rat hippocampus via activation of V(1A) receptors.

Gunasekaran Ramanathan, Nicholas I Cilz, Lalitha Kurada, Binqi Hu, Xiaoping Wang, Saobo Lei

Abstract read
In one paragraph

Article in Neuropharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Roles of PLCβ, PIPJournal of cellular physiology · 2022
    Article
  6. Article
  7. Activation of VNeuropharmacology · 2021
    Article
  8. Roles of KNeuropharmacology · 2019
    Article
  9. Review
  10. Vasopressin excites interneurons to suppress hippocampal network activity across a broad span of brain maturity at birth.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

6 authors at 1 institution in 1 country.

Gunasekaran RamanathanDepartment of Pharmacology, Physiology and Therapeutics, School of Medicine and Health Sciences, University of North Dakota, Grand Forks, ND 58203, USA.
Nicholas I Cilz
Lalitha Kurada
Binqi Hu
Xiaoping Wang
Saobo Lei
University of North Dakota · US

Funding

Roles and mechanisms of neurotensin in learning and memoryR01MH082881 · NIMH · UNIVERSITY OF NORTH DAKOTA · PI LEI, SAOBO · 2008 to 2015
$2.5M
NIMH NIH HHS MH082881NIMH NIH HHS R01 MH082881
6 · The paper itself

Abstract

Whereas vasopressin has been shown to enhance memory possibly by increasing long-term potentiation and direct excitation of the pyramidal neurons in the hippocampus, the effects of vasopressin on GABAergic transmission in the hippocampus remain to be determined. Here we examined the effects of vasopressin on GABAergic transmission onto CA1 pyramidal neurons and our results demonstrate that bath application of [Arg(8)]-vasopressin (AVP) dose-dependently increased the frequency of spontaneous IPSCs (sIPSCs) recorded from CA1 pyramidal neurons via activation of V(1A) receptors. Immunohistological staining and western blot further confirmed that both CA1 pyramidal neurons and interneurons expressed V(1A) receptors. Bath application of AVP altered neither the frequency nor the amplitude of miniature IPSCs in the presence of tetradotoxin and failed to change significantly the amplitude of evoked IPSCs recorded from CA1 pyramidal neurons. AVP increased the firing frequency of action potentials by depolarizing the GABAergic interneurons in the stratum radiatum of CA1 region. AVP-mediated depolarization of interneurons was mediated by inhibition of a background K(+) conductance which was insensitive to extracellular tetraethylammonium, Cs(+), 4-aminopyridine, tertiapin-Q and Ba(2+). AVP-induced depolarization of interneurons was dependent on Gα(q/11) but independent of phospholipase C, intracellular Ca(2+) release and protein kinase C. The inhibitory effects of AVP-mediated modulation of GABA release onto CA1 pyramidal neurons were overwhelmed by its strong excitation of CA1 pyramidal neurons in physiological condition but revealed when its direct excitation of the pyramidal neurons was blocked suggesting that AVP-mediated modulation of GABAergic transmission fine-tunes the excitability of CA1 pyramidal neurons.

Indexed as

Action PotentialsAnimalsgamma-Aminobutyric AcidHippocampusInhibitory Postsynaptic PotentialsMembrane PotentialsNeural InhibitionNeuronsPatch-Clamp TechniquesRatsRats, Sprague-DawleyReceptors, VasopressinSynapsesSynaptic TransmissionVasopressinsgamma-Aminobutyric AcidReceptors, VasopressinVasopressins

Identifiers

PMID22884625
PMCPMC3438289
OpenAlexW1995071454

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.