Evidence map›Paper›PMID 11410632›Full record

ArticleThe Journal of physiology2001

Photolysis-induced suppression of inhibition in rat hippocampal CA1 pyramidal neurons.

J Wang, R S Zucker

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

18 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Cannabinoid-mediated short-term plasticity in hippocampus.Journal of computational neuroscience · 2014
    Article
  3. Article
  4. Article
  5. Article
  6. Review
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  8. Article
  9. Review
  10. Somatic spikes regulate dendritic signaling in small neurons in the absence of backpropagating action potentials.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2009
    Article
  11. Article
  12. Article
  13. Endocannabinoid signaling dynamics probed with optical tools.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005
    Article
  14. Article
  15. Review
  16. Article
  17. Calcium dependence of retrograde inhibition by endocannabinoids at synapses onto Purkinje cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  18. Short-term retrograde inhibition of GABAergic synaptic currents in rat Purkinje cells is mediated by endogenous cannabinoids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2002
    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.

J WangDepartment of Molecular and Cell Biology, University of California, Berkeley, CA 94720, USA.
R S Zucker
University of California, Berkeley · US

Funding

REGULATION OF SYNAPTIC TRANSMISSIONR01NS015114 · NINDS · UNIVERSITY OF CALIFORNIA BERKELEY · PI ZUCKER, ROBERT STEPHEN · 1985 to 2002
$1.1M
NINDS NIH HHS NS 15114NINDS NIH HHS R01 NS015114
6 · The paper itself

Abstract

1. Whole cell patch clamp recording, Ca(2+) measurement with ratiometric fluorescent dyes and photolysis of caged Ca(2+) were combined to investigate the depolarization- and photolysis-induced suppression of inhibition (DSI and PSI) in rat hippocampal CA1 pyramidal cells. 2. A 5-s depolarization from -70 mV to 0 mV or a 6-s photolysis of nitrophenyl-EGTA (NPE) in cell bodies could each depress the frequency of spontaneous inhibitory postsynaptic currents (IPSCs) and the amplitude of evoked IPSCs while elevating intracellular Ca(2+) concentration ([Ca(2+)](i)). 3. Within a cell the elevation of [Ca(2+)](i) induced by depolarization was inversely related to that induced by photolysis, suggesting that higher [NPE] is more effective in releasing caged Ca(2+) but also increases buffer capacity to reduce [Ca(2+)](i) rises caused by Ca(2+) influx through voltage-dependent Ca(2+) channels. 4. Both DSI and PSI were linearly related to [Ca(2+)](i), with a 50 % reduction in transmission occurring at about 3.6--3.9 microM. 5. [Ca(2+)](i) recovered more quickly than DSI, indicating that the duration of DSI is not set simply by the duration of [Ca(2+)](i) elevation, but rather entails other rate-limiting processes. 6. We conclude that DSI is activated by micromolar [Ca(2+)](i) acting far from sites of Ca(2+) entry through channels in the plasma membrane.

Indexed as

PhotolysisAnimalsBuffersCalciumChelating AgentsEgtazic AcidElectrophysiologyHippocampusIntracellular MembranesIn Vitro TechniquesNeural InhibitionOsmolar ConcentrationPyramidal CellsRatsRats, Sprague-DawleySynaptic Transmission2-nitrophenyl-EGTABuffersCalciumChelating AgentsEgtazic Acid

Identifiers

PMID11410632
PMCPMC2278669
OpenAlexW2137935896

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.