Evidence map›Paper›PMID 11118504›Full record

ArticleThe Journal of physiology2000

Re-evaluation of phorbol ester-induced potentiation of transmitter release from mossy fibre terminals of the mouse hippocampus.

I Honda, H Kamiya, H Yawo

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in The Journal of physiology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.5field-weighted citation impact, top 19% 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

15 citing papers in PubMed, 45 citations in OpenAlex.

  1. Pre- versus Post-synaptic Forms of LTP in Two Branches of the Same Hippocampal Afferent.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  2. Article
  3. Target-Dependent Compartmentalization of the Corelease of Glutamate and GABA from the Mossy Fibers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  4. Calcium-Dependent Protein Kinase C Is Not Required for Post-Tetanic Potentiation at the Hippocampal CA3 to CA1 Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Functional uncoupling between Ca2+ release and afterhyperpolarization in mutant hippocampal neurons lacking junctophilins.Proceedings of the National Academy of Sciences of the United States of America · 2006
    Article
  10. Article
  11. Article
  12. Review
  13. Presynaptic Ca2+ entry is unchanged during hippocampal mossy fiber long-term potentiation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    Article
  14. Paired-pulse plasticity at the single release site level: an experimental and computational study.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  15. 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 3 institutions in 1 country.

I HondaDepartment of Neurophysiology, Tohoku University School of Medicine, Sendai 980-8575, Japan.
H Kamiya
H Yawo
Gunma University · JPJapan Science and Technology Agency · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

To investigate the mechanisms by which phorbol esters potentiate transmitter release from mossy fibre terminals we used fura dextran to measure the intraterminal Ca2+ concentration in mouse hippocampal slices. A phorbol ester, phorbol 12,13-diacetate (PDAc), potentiated the field excitatory postsynaptic potential (fEPSP) slope. PDAc also enhanced the stimulation-dependent increase of [Ca2+]i in the mossy fibre terminal (Delta[Ca2+]pre). The magnitude of the PDAc-induced fEPSP potentiation (463+/-57% at 10 microM) was larger than that expected from the enhancement of Delta[Ca2+]pre (153+/-5%). The Delta[Ca2+]pre was suppressed by omega-agatoxin IVA (omega-AgTxIVA, 200 nM), a P/Q-type Ca2+ channel-specific blocker, by 31%. The effect of PDAc did not select between omega-AgTxIVA-sensitive and -resistant components. The PDAc-induced potentiation of the fEPSP slope was partially antagonized by the protein kinase C (PKC) inhibitor bisindolylmaleimide I (BIS-I, 10 microM), whereas the Delta[Ca2+]pre was completely blocked by BIS-I. Although the BIS-I-sensitive fEPSP potentiation was accompanied by a reduction of the paired-pulse ratio (PPR), the BIS-I-resistant component was not. Whole-cell patch clamp recording from a CA3 pyramidal neuron in a BIS-I-treated slice demonstrated that PDAc (10 microM) increased the frequency of miniature excitatory postsynaptic currents (mEPSCs, 259+/-33% of control) without a noticeable change in their amplitude (102+/-5% of control). These results suggest that PKC potentiates transmitter release by at least two distinct mechanisms, one Delta[Ca2+]pre dependent and the other Delta[Ca2+]pre independent. In addition, some phorbol ester-mediated potentiation of synaptic transmission appears to occur without activating PKC.

Indexed as

Action PotentialsAnimalsCalciumCalcium Channel BlockersExcitatory Postsynaptic PotentialsIndolesIn Vitro TechniquesMaleimidesMiceMossy Fibers, HippocampalNerve EndingsNeurotransmitter Agentsomega-Agatoxin IVAomega-Conotoxin GVIAOsmolar ConcentrationPhorbol Estersbisindolylmaleimide ICalciumCalcium Channel BlockersIndolesMaleimidesNeurotransmitter Agentsomega-Agatoxin IVAomega-Conotoxin GVIAphorbol-12,13-diacetatePhorbol EstersProtein Kinase C

Identifiers

PMID11118504
PMCPMC2270214
OpenAlexW2089105518

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.