Evidence map›Paper›PMID 12917362›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Presynaptic and postsynaptic mechanisms of a novel form of homosynaptic potentiation at aplysia sensory-motor neuron synapses.

Iksung Jin, Robert D Hawkins

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–field-weighted citation impact
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

32 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Hyperpolarization-activated, cyclic nucleotide-gated cation channels in Aplysia: Contribution to classical conditioning.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  6. Article
  7. Nonassociative learning in invertebrates.Cold Spring Harbor perspectives in biology · 2015
    Review
  8. Article
  9. Persistent long-term facilitation at an identified synapse becomes labile with activation of short-term heterosynaptic plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  10. Article
  11. Review
  12. Article
  13. Spontaneous transmitter release is critical for the induction of long-term and intermediate-term facilitation in Aplysia.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  14. Spontaneous transmitter release recruits postsynaptic mechanisms of long-term and intermediate-term facilitation in Aplysia.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  15. Site-specific synapsin I phosphorylation participates in the expression of post-tetanic potentiation and its enhancement by BDNF.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  16. Rapid increase in clusters of synaptophysin at onset of homosynaptic potentiation in Aplysia.Proceedings of the National Academy of Sciences of the United States of America · 2011
    Article
  17. Differential control of presynaptic CaMKII activation and translocation to active zones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  18. Article
  19. Article
  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.

Iksung JinCenter for Neurobiology and Behavior, Columbia University, and New York State Psychiatric Institute, New York, New York 10032, USA.
Robert D Hawkins

Funding

LEARNING MECHANISMS IN THE ABDOMINAL GANGLIONR01MH026212 · NIMH · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI HAWKINS, ROBERT D · 1985 to 2003
$829k
NIMH NIH HHS MH26212NIMH NIH HHS R01 MH026212
6 · The paper itself

Abstract

Previous studies have shown that homosynaptic potentiation produced by rather mild tetanic stimulation (20 Hz, 2 sec) at Aplysia sensory-motor neuron synapses in isolated cell culture involves both presynaptic and postsynaptic Ca2+ (Bao et al., 1997). We have now investigated the sources of Ca2+ and some of its downstream targets. Although the potentiation lasts >30 min, it does not require Ca2+ influx through either NMDA receptor channels or L-type Ca2+ channels. Rather, the potentiation involves metabotropic receptors and intracellular Ca2+ release from both postsynaptic IP3-sensitive and presynaptic ryanodine-sensitive stores. In addition, it involves protein kinases, including both presynaptic and postsynaptic CamKII and probably MAP kinase. Finally, it does not require transsynaptic signaling by nitric oxide but it may involve AMPA receptor insertion. The potentiation, thus, shares components of the mechanisms of post-tetanic potentiation, NMDA- and mGluR-dependent long-term potentiation, and even long-term depression, but is not identical to any of them. These results are consistent with the more general idea that there is a molecular alphabet of basic components that can be combined in various ways to create novel as well as known types of plasticity.

Indexed as

Neuronal PlasticityAnimalsAplysiaCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium ChannelsCoculture TechniquesInositol 1,4,5-Trisphosphate ReceptorsIon TransportLong-Term PotentiationMAP Kinase Signaling SystemMotor NeuronsNeurons, AfferentNitric OxideProtein KinasesCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium ChannelsInositol 1,4,5-Trisphosphate ReceptorsNitric OxideProtein KinasesReceptors, AMPAReceptors, Cytoplasmic and NuclearReceptors, N-Methyl-D-AspartateReceptors, PresynapticRyanodine Receptor Calcium Release Channel

Identifiers

PMID12917362
PMCPMC6740441

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.