Evidence map›Paper›PMID 23485803›Full record

ArticleNeuroscience2013

Astrocytes release D-serine by a large vesicle.

N Kang, H Peng, Y Yu, P K Stanton, T R Guilarte, J Kang

Abstract read
In one paragraph

Article in Neuroscience, 2013. 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
4.8field-weighted citation impact, top 5% 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, 56 citations in OpenAlex.

  1. Review
  2. The role of astrocytes in depression, its prevention, and treatment by targeting astroglial gliotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. NMDARs, Coincidence Detectors of Astrocytic and Neuronal Activities.International journal of molecular sciences · 2021
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Gliocrine System: Astroglia as Secretory Cells of the CNS.Advances in experimental medicine and biology · 2019
    Review
  13. Review
  14. Article
  15. Physiology of Astroglia.Physiological reviews · 2018
    Review
  16. The Neuroglial Dialog Between Cannabinoids and Hemichannels.Frontiers in molecular neuroscience · 2018
    Article
  17. Contribution of Astroglial Cx43 Hemichannels to the Modulation of Glutamatergic Currents by D-Serine in the Mouse Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  18. Article
  19. Review
  20. 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

6 authors at 2 institutions in 1 country.

N KangDepartment of Cell Biology and Anatomy, New York Medical College, Basic Science Building, Room 220, Valhalla, NY 10595, USA.
H Peng
Y Yu
P K Stanton
T R Guilarte
J Kang
New York Medical College · USColumbia University · US

Funding

NMDA RECEPTOR FUNCTION IN LEAD NEUROTOXICITYR01ES006189 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI GUILARTE, TOMAS R · 1993 to 2019
$9.3M
TSPO and Neuroinflammation in Alzheimer's DiseaseR01ES007062 · NIEHS · JOHNS HOPKINS UNIVERSITY · PI GUILARTE, TOMAS R · 1995 to 2023
$7.3M
NIEHS NIH HHS ES006189NIEHS NIH HHS R01 ES006189NIEHS NIH HHS R01 ES007062
6 · The paper itself

Abstract

Long-term potentiation (LTP) of synaptic transmission in the CA1 region of the hippocampus depends on the activation of N-methyl-D-aspartate receptors (NMDARs), which can be regulated by Ca²⁺-dependent release of D-serine from astrocytes. The detailed mechanism underlying astrocytic d-serine release is still unknown. In hippocampal slices prepared from Sprague-Dawley rats, we found that clamping astrocytic [Ca²⁺] at 100-150 nM or puffing artificial cerebrospinal fluid (ACSF) into the extracellular space (weak mechanical stimulation) enhanced the synaptic activation of NMDARs. The enhancement was blocked by the NMDAR glycine site antagonist 5,7-dichlorokynurenic acid, glycine saturation, and infusion of astrocytes with D-amino acid oxidase and the serine racemase inhibitor L-erythro-3-hydroxyaspartate, suggesting the involvement of astrocytic D-serine release. Intracellular 100-150 nM [Ca²⁺] or puffing ACSF stimulated astrocytes to generate D-serine-containing large vesicles (1-3 μm), exocytotic fusion of which released D-serine. The formation of astrocytic large vesicles involved the intracellular fusion of small vesicles and/or other organelles. Spontaneous fusion of large vesicles occurred occasionally in astrocytes at rest, contributing to baseline D-serine levels, which increased the rising slope of NMDAR post-burst potentiation (PBP) without altering the PBP peak amplitude. Thus, under physiological conditions, astrocytic D-serine release by large vesicles facilitated weak theta-burst (TBS consisting of five bursts), but not strong TBS (TBS consisting of 10 bursts) stimulation-induced LTP.

Indexed as

Adenosine DiphosphateAnimalsAnimals, NewbornAspartic AcidAstrocytesBiophysicsCalciumCytoplasmic VesiclesDose-Response Relationship, DrugElectric StimulationExcitatory Amino Acid AgentsExcitatory Postsynaptic PotentialsExocytosisFemaleGlycineHippocampus2-amino-5-phosphopentanoic acid3-hydroxyaspartic acidAdenosine DiphosphateAspartic AcidCalciumExcitatory Amino Acid AgentsGlycineN(6)-methyl-2'-deoxyadenosine 3',5'-diphosphatePurinergic P2Y Receptor AntagonistsSerineValine

Identifiers

PMID23485803
PMCPMC4335764
OpenAlexW1964835919

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.