Evidence map›Paper›PMID 18685024›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008

Application of an Epac activator enhances neurotransmitter release at excitatory central synapses.

Isabella Gekel, Erwin Neher

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

52 citing papers in PubMed, 98 citations in OpenAlex.

  1. Article
  2. A specific negatively charged sequence confers intramolecular regulation on Munc13-1 function in synaptic exocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  3. Article
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  5. Fully-primed slowly-recovering vesicles mediate presynaptic LTP at neocortical neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  6. Article
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  8. Article
  9. Review
  10. Article
  11. Glycine Release Is Potentiated by cAMP via EPAC2 and CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  12. Axonal CB1 Receptors Mediate Inhibitory Bouton Formation via cAMP Increase and PKA.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  13. Synapsin Is Required for Dense Core Vesicle Capture and cAMP-Dependent Neuropeptide Release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. Autaptic Cultures: Methods and Applications.Frontiers in synaptic neuroscience · 2020
    Article
  18. Review
  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

2 authors at 1 institution in 1 country.

Isabella GekelDepartment of Membrane Biophysics, Max Planck Institute for Biophysical Chemistry, 37077 Göttingen, Germany.
Erwin Neher
Max Planck Institute for Biophysical Chemistry · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

cAMP regulates secretory processes through both PKA-independent and PKA-dependent signaling pathways. Their relative contributions to fast neurotransmission are unclear at present, although forskolin, which is generally believed to enhance intracellular cAMP levels by stimulation of adenylyl cyclase activity, was shown to increase vesicular release probability (p) and the number of releasable vesicles (N) in various neuronal preparations. Using low-frequency (0.2 Hz) electrophysiological recordings in the presence of the Epac-selective cAMP analog 8-pCPT-2'-O-Me-cAMP (ESCA(1)), we find that Epac activation by this analog accounts on average for 38% of the forskolin-induced increase in evoked EPSC amplitudes and for 100% of the forskolin-induced increase in miniature EPSC (mEPSC) frequency in dissociated autaptic neuronal cultures from mouse hippocampus. From paired-pulse facilitation experiments, and considering the enhancement of mEPSC frequency, we conclude that ESCA(1)-induced Epac activity is presynaptic in origin and increases p. In addition, preapplication of ESCA(1) augmented a subsequent enhancement of evoked EPSC amplitudes by phorbol ester (PDBu). This effect was maximal when ESCA(1) application preceded the PDBu application by 3 min. Because the PDBu response was abolished after downregulation of intracellular PKC activity, we conclude that ESCA(1)-induced Epac activation leads to presynaptic changes involving Epac-to-PKC signaling.

Indexed as

AnimalsCells, CulturedCyclic AMPDrug Administration ScheduleExcitatory Postsynaptic PotentialsGuanine Nucleotide Exchange FactorsHippocampusMiceNeurotransmitter AgentsPhorbol 12,13-DibutyrateProbabilityProtein IsoformsProtein Kinase CRatsSignal TransductionSpecies Specificity8-(4-chloro-phenylthio)-2'-O-methyladenosine-3'-5'-cyclic monophosphateCyclic AMPEpac protein, mouseGuanine Nucleotide Exchange FactorsNeurotransmitter AgentsPhorbol 12,13-DibutyrateProtein IsoformsProtein Kinase CRapgef3 protein, rat

Identifiers

PMID18685024
PMCPMC6670779
OpenAlexW2150377079

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.