Evidence map›Paper›PMID 23637168›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Presynaptic NMDA receptor mechanisms for enhancing spontaneous neurotransmitter release.

Portia A Kunz, Adam C Roberts, Benjamin D Philpot

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 64 citations in OpenAlex.

  1. Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Reduction of the CaFrontiers in cellular neuroscience · 2025
    Review
  4. Article
  5. GluN2A- and GluN2B-containing pre-synapticPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Advances and Barriers in Understanding PresynapticFrontiers in molecular neuroscience · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Portia A KunzDepartment of Cell Biology and Physiology, Carolina Institute for Developmental Disabilities, Neuroscience Center, and Curriculum in Neurobiology, University of North Carolina, Chapel Hill, North Carolina, 27599-7545, USA.
Adam C Roberts
Benjamin D Philpot
University of North Carolina at Chapel Hill · US

Funding

Postdoctoral Research in Neurodevelopmental DisordersT32HD040127 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI BENJAMIN D PHILPOT, Mark D Shen · 2001 to 2026
$8.5M
Mechanisms of Presynaptic Plasticity in Visual CortexR01EY018323 · NEI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI PHILPOT, BENJAMIN D · 2007 to 2011
$1.8M
NEI NIH HHS R01 EY018323NEI NIH HHS R01EY018323NICHD NIH HHS T32 HD040127NICHD NIH HHS T32-HD40127
6 · The paper itself

Abstract

NMDA receptors (NMDARs) are required for experience-driven plasticity during formative periods of brain development and are critical for neurotransmission throughout postnatal life. Most NMDAR functions have been ascribed to postsynaptic sites of action, but there is now an appreciation that presynaptic NMDARs (preNMDARs) can modulate neurotransmitter release in many brain regions, including the neocortex. Despite these advances, the cellular mechanisms by which preNMDARs can affect neurotransmitter release are largely unknown. Here we interrogated preNMDAR functions pharmacologically to determine how these receptors promote spontaneous neurotransmitter release in mouse primary visual cortex. Our results provide three new insights into the mechanisms by which preNMDARs can function. First, preNMDARs can enhance spontaneous neurotransmitter release tonically with minimal extracellular Ca(2+) or with major sources of intracellular Ca(2+) blocked. Second, lowering extracellular Na(+) levels reduces the contribution of preNMDARs to spontaneous transmitter release significantly. Third, preNMDAR enhance transmitter release in part through protein kinase C signaling. These data demonstrate that preNMDARs can act through novel pathways to promote neurotransmitter release in the absence of action potentials.

Indexed as

2-Amino-5-phosphonovalerateAnimalsAnimals, NewbornCalciumCerebral CortexDose-Response Relationship, DrugElectric StimulationEnzyme InhibitorsExcitatory Amino Acid AntagonistsExcitatory Postsynaptic PotentialsFemaleIn Vitro TechniquesMaleMiceMice, Inbred C57BLNeurons2-Amino-5-phosphonovalerateCalciumEnzyme InhibitorsExcitatory Amino Acid AntagonistsICI D2788Neurotransmitter AgentsPyrimidinesReceptors, N-Methyl-D-AspartateSodium Channel BlockersSodium ChlorideTetrodotoxin

Identifiers

PMID23637168
PMCPMC3688260
OpenAlexW2071495374

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.