Evidence map›Paper›PMID 10377331›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

A zinc-dependent Cl- current in neuronal somata.

T Tabata, A T Ishida

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.6field-weighted citation impact, top 37% 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

9 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Zinc in the Brain: Friend or Foe?International journal of molecular sciences · 2020
    Review
  3. Review
  4. Article
  5. Article
  6. Dissociation of retinal ganglion cells without enzymes.Journal of neuroscience methods · 2004
    Article
  7. Article
  8. A dopamine- and protein kinase A-dependent mechanism for network adaptation in retinal ganglion cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001
    Article
  9. Deactivation, recovery from inactivation, and modulation of extra-synaptic ion currents in fish retinal ganglion cells.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2000
    Review
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.

T TabataSection of Neurobiology, Physiology, and Behavior, University of California, Davis, 95616-8519, USA.
A T Ishida
University of California, Davis · US

Funding

PHARMACOLOGY &PHYSIOLOGY OF RETINAL GANGLION CELLSR01EY008120 · NEI · UNIVERSITY OF CALIFORNIA DAVIS · PI ISHIDA, ANDREW T · 1995 to 2017
$6.7M
PHARMACOLOGY AND PHYSIOLOGY OF RETINAL GANGLION CELLSR29EY008120 · NEI · UNIVERSITY OF CALIFORNIA DAVIS · PI ISHIDA, ANDREW T · 1989 to 1993
–
NEI NIH HHS EY 08120NEI NIH HHS R01 EY008120
6 · The paper itself

Abstract

Extracellular Zn2+ modulates current passage through voltage- and neurotransmitter-gated ion channels, at concentrations less than, or near, those produced by release at certain synapses. Electrophysiological effects of cytoplasmic Zn2+ are less well understood, and effects have been observed at concentrations that are orders of magnitude greater than those found in resting and stimulated neurons. To examine whether and how neurons are affected by lower levels of cytoplasmic Zn2+, we tested the effect of Zn2+-selective chelators, Zn2+-preferring ionophores, and exogenous Zn2+ on neuronal somata during whole-cell patch-clamp recordings. We report here that cytoplasmic zinc facilitates the downward regulation of a background Cl- conductance by an endogenous protein kinase C (PKC) in fish retinal ganglion cell somata and that this regulation is maintained if nanomolar levels of free Zn2+ are available. This regulation has not been described previously in any tissue, as other Cl- currents have been described as reduced by PKC alone, reduced by Zn2+ alone, or reduced by both independently. Moreover, control of cation currents by a zinc-dependent PKC has not been reported previously. The regulation we have observed thus provides the first electrophysiological measurements consistent with biochemical measurements of zinc-dependent PKC activity in other systems. These results suggest that contributions of background Cl- conductances to electrical properties of neurons are susceptible to modulation.

Indexed as

Ion Channel Gating4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic AcidAnimalsCalciumCationsChelating AgentsChloridesCyclic AMPCytoplasmEnzyme ActivationGoldfishIndolesIon ChannelsIonophoresMaleimides4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfonic Acidadenosine-3',5'-cyclic phosphorothioatebisindolylmaleimideCalciumcalphostin CCationsChelating AgentsChloridesCyclic AMPIndolesIon ChannelsIonophoresMaleimidesNaphthalenesProtein Kinase CThionucleotidesZinc

Identifiers

PMID10377331
PMCPMC6782341
OpenAlexW1955565432

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.