Evidence map›Paper›PMID 16537522›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

G protein betagamma-subunits activated by serotonin mediate presynaptic inhibition by regulating vesicle fusion properties.

Huzefa Photowala, Trillium Blackmer, Eric Schwartz, Heidi E Hamm, Simon Alford

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.9field-weighted citation impact, top 10% 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, 75 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Single Calcium Channel Nanodomains Drive Presynaptic Calcium Entry at Lamprey Reticulospinal Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  6. Synaptic Integration of Subquantal Neurotransmission by Colocalized G Protein-Coupled Receptors in Presynaptic Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. GPCR regulation of secretion.Pharmacology & therapeutics · 2018
    Review
  13. Synaptic Vesicle Endocytosis in Different Model Systems.Frontiers in cellular neuroscience · 2018
    Review
  14. Article
  15. Article
  16. Accumulation of KThe Journal of physiology · 2017
    Article
  17. Article
  18. Review
  19. Review
  20. Cannabinoids and Epilepsy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2015
    Review
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

5 authors at 3 institutions in 2 countries.

Huzefa PhotowalaDepartment of Biological Sciences, University of Illinois, 840 West Taylor Street, Chicago, IL 60607, USA.
Trillium Blackmer
Eric Schwartz
Heidi E Hamm
Simon Alford
University of Illinois Chicago · USOregon Health & Science University · USVanderbilt University · US

Funding

Molecular basis of GPCR-mediated presynaptic inhibitionR01MH064763 · NIMH · UNIVERSITY OF ILLINOIS AT CHICAGO · PI ALFORD, SIMON T · 2002 to 2005
$903k
NIMH NIH HHS R01 MH064763
6 · The paper itself

Abstract

Neurotransmitters are thought to be released as quanta, where synaptic vesicles deliver packets of neurotransmitter to the synaptic cleft by fusion with the plasma membrane. However, synaptic vesicles may undergo incomplete fusion. We provide evidence that G protein-coupled receptors inhibit release by causing such incomplete fusion. 5-hydroxytryptamine (5-HT) receptor signaling potently inhibits excitatory postsynaptic currents (EPSCs) between lamprey reticulospinal axons and their postsynaptic targets by a direct action on the vesicle fusion machinery. We show that 5-HT receptor-mediated presynaptic inhibition, at this synapse, involves a reduction in EPSC quantal size. Quantal size was measured directly by comparing unitary quantal amplitudes of paired EPSCs before and during 5-HT application and indirectly by determining the effect of 5-HT on the relationship between mean-evoked EPSC amplitude and variance. Results from FM dye-labeling experiments indicate that 5-HT prevents full fusion of vesicles. 5-HT reduces FM1-43 staining of vesicles with a similar efficacy to its effect on the EPSC. However, destaining of FM1-43-labeled vesicles is abolished by lower concentrations of 5-HT that leave a substantial EPSC. The use of a water-soluble membrane impermeant quenching agent in the extracellular space reduced FM1-43 fluorescence during stimulation in 5-HT. Thus vesicles contact the extracellular space during inhibition of synaptic transmission by 5-HT. We conclude that 5-HT, via free Gbetagamma, prevents the collapse of synaptic vesicles into the presynaptic membrane.

Indexed as

AnimalsExcitatory Postsynaptic PotentialsGTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsIn Vitro TechniquesMembrane FusionPetromyzonReceptors, SerotoninSerotoninSynaptic TransmissionSynaptic VesiclesGTP-Binding Protein beta SubunitsGTP-Binding Protein gamma SubunitsReceptors, SerotoninSerotonin

Identifiers

PMID16537522
PMCPMC1449684
OpenAlexW2063321702

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.