Evidence map›Paper›PMID 16738253›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

Exocytosis of vesicular zinc reveals persistent depression of neurotransmitter release during metabotropic glutamate receptor long-term depression at the hippocampal CA3-CA1 synapse.

Jing Qian, Jeffrey L Noebels

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 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
2.0field-weighted citation impact, top 15% 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, 73 citations in OpenAlex.

  1. Synaptotagmin-1 serves as a primary ZnNature communications · 2025
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Synaptic Zinc: An Emerging Player in Parkinson's Disease.International journal of molecular sciences · 2021
    Review
  7. CaChannels (Austin, Tex.) · 2020
    Review
  8. Zinc in the Brain: Friend or Foe?International journal of molecular sciences · 2020
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Modulation of extrasynaptic NMDA receptors by synaptic and tonic zinc.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  18. Article
  19. Article
  20. Synaptic Zn2+ inhibits neurotransmitter release by promoting endocannabinoid synthesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 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

2 authors at 1 institution in 1 country.

Jing QianDepartment of Neurology, Baylor College of Medicine, Houston, Texas 77030, USA.
Jeffrey L Noebels
Baylor College of Medicine · US

Funding

PLASTICITY IN DEVELOPING EPILEPTIC BRAINR01NS029709 · NINDS · BAYLOR COLLEGE OF MEDICINE · PI NOEBELS, JEFFREY · 1991 to 2025
$9.1M
NINDS NIH HHS NS29709
6 · The paper itself

Abstract

Exocytosis can be directly measured in mammalian brain slices by fluorescence detection of vesicular zinc release. Detection of the low-level evoked zinc signal [Zn]t was first demonstrated at the zinc-rich hippocampal mossy fiber pathway and required the use of high-frequency presynaptic stimulation. Here, we show that release after individual action potentials can be reliably detected even at non-mossy fiber, zinc-poor synapses in the hippocampus, a major enhancement in the temporal resolution of the technique. Short-term facilitation of release properties of zinc-positive CA3-CA1 Schaffer collateral/commissural synapses in the stratum radiatum differ from those at mossy fibers but are similar to those measured for the EPSP [field EPSP (fEPSP)]. The N-type Ca2+ channel toxin omega-conotoxin GVIA inhibited both the [Zn]t and fEPSP equally, and the modulation of neurotransmitter release by neuropeptide Y, baclofen, and adenosine as revealed by [Zn]t closely resembles that measured for the fEPSP. A long-standing controversy in hippocampal synaptic plasticity involves the site of long-term depression (LTD) at these synapses. Using zinc release as a direct marker for exocytotic events and a surrogate marker for glutamate release, we demonstrate that persistent depression of presynaptic release occurs in the late expression of DHPG [(S)-3,5-dihydroxyphenylglycine]-induced LTD at this synapse. The ability to examine release dynamics with zinc fluorescence detection will facilitate exploration of the molecular pharmacology and plasticity of exocytosis at many CNS synapses.

Indexed as

Action PotentialsAdenosineAnimalsBaclofenCarrier ProteinsCation Transport ProteinsCrosses, GeneticExcitatory Postsynaptic PotentialsExocytosisHippocampusLong-Term Synaptic DepressionMembrane ProteinsMembrane Transport ProteinsMiceMice, Inbred C57BLMice, KnockoutAdenosineBaclofenCarrier ProteinsCation Transport ProteinsMembrane ProteinsMembrane Transport ProteinsNeuropeptide YNeurotransmitter AgentsReceptors, Metabotropic GlutamateSlc30a3 protein, mouseZinc

Identifiers

PMID16738253
PMCPMC6675221
OpenAlexW1972834856

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.