Evidence map›Paper›PMID 11102462›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000

Independence of and interactions between GABA-, glutamate-, and acetylcholine-activated Cl conductances in Aplysia neurons.

J Kehoe, C Vulfius

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. Characterization of Brain Dysfunction Induced by Bacterial Lipopeptides That Alter Neuronal Activity and Network in Rodent Brains.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Acetylcholine receptors in spider peripheral mechanosensilla.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2006
    Article
  8. Article
  9. Concerted GABAergic actions of Aplysia feeding interneurons in motor program specification.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003
    Article
  10. The shift of the reversal potential of glutamate-activated chloride current in molluscan neurons caused by 8-Br-cAMP.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections
    Article
  11. Long-term potentiation of the glutamate-activated inward current induced by 8-Br-cGMP in nerve cell.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections
    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 2 institutions in 2 countries.

J KehoeLaboratoire de Neurobiologie, Ecole Normale Supérieure, Paris 75005, France. kehoe@wotan.ens.fr
C Vulfius
Institute of Cell Biophysics · RULaboratoire de Géologie de l’École Normale Supérieure · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In certain Aplysia neurons, glutamate, GABA, and acetylcholine (ACh) all elicit desensitizing Cl-dependent responses. This fact and the finding that the glutamate and GABA responses "cross-desensitize" led to the suggestion (Swann and Carpenter, 1975; King and Carpenter, 1987) that the responses to these transmitters were mediated by the same receptor-channel complex. This hypothesis is incompatible with the demonstration given here that the GABA- and glutamate-gated channels are clearly distinct; the GABA channel, but not the glutamate channel, shows outward rectification (Matsumoto, 1982; King and Carpenter, 1987, 1989) and is selectively blocked by intracellular sulfate. Exploiting these distinctive characteristics and the independent expression of the receptors in some cells, we have been able to reevaluate the so-called cross-desensitization by analyzing the ability of GABA, glutamate, and other agonists to interact with each of the receptor molecules. The cross-desensitization was found to be exclusively attributable to the ability of GABA to interact with the glutamate receptor (Oyama et al., 1990). The GABA receptor is unaffected by glutamate. Nevertheless, in cells expressing both receptors, glutamate can reduce the GABA response by auto-desensitizing the part of the response that is mediated by the glutamate receptor. No interactions were observed between ACh-induced responses and either of the responses elicited by the amino acids. The invertebrate glutamate-gated Cl channels that have been cloned resemble the vertebrate glycine receptor (Vassilatis et al., 1997). Our pharmacological evaluation of the molluscan glutamate receptor points in the same direction.

Indexed as

AcetylcholineAnimalsAplysiabeta-AlanineCells, CulturedChloride ChannelsChloridesCrotonatesDose-Response Relationship, DrugExcitatory Amino Acid Agentsgamma-Aminobutyric AcidGanglia, InvertebrateGlutamic AcidIn Vitro TechniquesIon Channel GatingNeurons4-aminocrotonic acidAcetylcholinebeta-AlanineChloride ChannelsChloridesCrotonatesExcitatory Amino Acid Agentsgamma-Aminobutyric AcidGlutamic AcidhypotaurineReceptors, CholinergicReceptors, GABAReceptors, GlutamateSulfatesTaurine

Identifiers

PMID11102462
PMCPMC6773048
OpenAlexW2114235659

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.