Evidence map›Paper›PMID 9782165›Full record

ArticleThe Journal of physiology1998

Transmitter release modulation in nerve terminals of rat neocortical pyramidal cells by intracellular calcium buffers.

O Ohana, B Sakmann

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

51 citing papers in PubMed, 90 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Upregulated CaCells · 2022
    Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Mechanisms and Functional Consequences of Presynaptic Homeostatic Plasticity at Auditory Nerve Synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  11. Suppression of Presynaptic Glutamate Release by Postsynaptic Metabotropic NMDA Receptor Signalling to Pannexin-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  12. Synaptotagmin CaFrontiers in molecular neuroscience · 2018
    Review
  13. Article
  14. Intracellular,The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  15. Article
  16. Developmental tightening of cerebellar cortical synaptic influx-release coupling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  17. Review
  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 at 1 institution in 1 country.

O OhanaAbteilung Zellphysiologie, Max-Planck-Institut fur medizinische Forschung, Jahnstrasse 29, D-69120 Heidelberg, Germany.
B Sakmann
Max Planck Society · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Dual whole-cell voltage recordings were made from synaptically connected layer 5 (L5) pyramidal neurones in slices of the young (P14-P16) rat neocortex. The Ca2+ buffers BAPTA or EGTA were loaded into the presynaptic neurone via the pipette recording from the presynaptic neurone to examine their effect on the mean and the coefficient of variation (c.v.) of single fibre EPSP amplitudes, referred to as unitary EPSPs. 2. The fast Ca2+ buffer BAPTA reduced unitary EPSP amplitudes in a concentration dependent way. With 0.1 mM BAPTA in the pipette, the mean EPSP amplitude was reduced by 14 +/- 2.8% (mean +/- s.e.m., n = 7) compared with control pipette solution, whereas with 1.5 mM BAPTA, the mean EPSP amplitude was reduced by 72 +/- 1.5% (n = 5). The concentration of BAPTA that reduced mean EPSP amplitudes to one-half of control was close to 0.7 mM. 3. Saturation of BAPTA during evoked release was tested by comparing the effect of loading the presynaptic neurone with 0.1 mM BAPTA at 2 and 1 mM [Ca2+]o. Reducing [Ca2+]o from 2 to 1 mM, thereby reducing Ca2+ influx into the terminals, decreased the mean EPSP amplitude by 60 +/- 2.2% with control pipette solution and by 62 +/- 1.9% after loading with 0.1 mM BAPTA (n = 7). 4. The slow Ca2+ buffer EGTA at 1 mM reduced mean EPSP amplitudes by 15 +/- 2.5% (n = 5). With 10 mM EGTA mean EPSP amplitudes were reduced by 56 +/- 2.3 % (n = 4). 5. With both Ca2+ buffers, the reduction in mean EPSP amplitudes was associated with an increase in the c.v. of peak EPSP amplitudes, consistent with a reduction of the transmitter release probability as the major mechanism underlying the reduction of the EPSP amplitude. 6. The results suggest that in nerve terminals of thick tufted L5 pyramidal cells the endogenous mobile Ca2+ buffer is equivalent to less than 0.1 mM BAPTA and that at many release sites of pyramidal cell terminals the Ca2+ channel domains overlap, a situation comparable with that at large calyx-type terminals in the brainstem.

Indexed as

AlgorithmsAnimalsCalciumChelating AgentsEgtazic AcidElectric StimulationElectrophysiologyExcitatory Postsynaptic PotentialsIn Vitro TechniquesMembrane PotentialsNeocortexNerve EndingsNeurotransmitter AgentsPatch-Clamp TechniquesPyramidal CellsRats1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidCalciumChelating AgentsEgtazic AcidNeurotransmitter Agents

Identifiers

PMID9782165
PMCPMC2231265
OpenAlexW1978936152

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.