Evidence map›Paper›PMID 9660895›Full record

ArticleThe Journal of physiology1998

Expression of functional GABAA receptors in cholecystokinin-secreting gut neuroendocrine murine STC-1 cells.

G Glassmeier, K H Herzig, M Höpfner, K Lemmer, A Jansen, H Scherubl

Open access · greenAbstract 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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Nutrient Combinations Sensed by L-Cell Receptors Potentiate GLP-1 Secretion.International journal of molecular sciences · 2024
    Article
  4. Article
  5. Article
  6. Role of the brain-gut axis in gastrointestinal cancer.World journal of clinical cases · 2019
    Review
  7. Article
  8. Stimulation of incretin secreting cells.Therapeutic advances in endocrinology and metabolism · 2016
    Review
  9. Article
  10. Article
  11. Molecular and functional diversity of GABA-A receptors in the enteric nervous system of the mouse colon.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  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

6 authors at 3 institutions in 2 countries.

G GlassmeierDepartment of Gastroenterology, Universitatsklinikum Benjamin Franklin, Freie Universitat Berlin, Germany.
K H Herzig
M Höpfner
K Lemmer
A Jansen
H Scherubl
Franklin University · USFreie Universität Berlin · DEKiel University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. Gastrointestinal neuroendocrine (NE) cells synthesize, store and secrete gamma-aminobutyric acid (GABA). Recently, an autocrine-paracrine function of GABA has been proposed for secretion from NE cells. 2. To search for functional GABAA receptors in NE gut cells, we performed whole-cell and perforated-patch-clamp studies in the intestinal cholecystokinin (CCK)-secreting NE cell line STC-1. 3. Application of GABA evoked currents in STC-1 cells. These effects were mimicked by muscimol, an agonist of GABAA receptors, and blocked by picrotoxin or bicuculline, antagonists of GABAA receptors. The GABA- or muscimol-activated currents reversed near 0 mV, which under the recording conditions used was consistent with the activation of the GABAA receptor-Cl- channel complex. 4. In contrast to the effect on most neurons, GABA as well as muscimol led to a (reversible) depolarization of the membrane potential of STC-1 cells. Membrane depolarization in turn activated voltage-gated Ca2+ channels and increased intracellular Ca2+ concentrations in STC-1 cells. 5. In accordance with the observed membrane depolarization and activation of voltage-gated Ca2+ channels, both GABA and muscimol stimulated Ca2+-dependent CCK release. In contrast, bicuculline inhibited the GABA-induced secretion of CCK. 6. Using the reverse transcription-polymerase chain reaction (RT-PCR), mRNA of the GABAA receptor subunits alpha2, alpha3, alpha5, beta1, beta3 and delta could be detected in STC-1 cells. 7. In summary, we have shown that the CCK-secreting gut NE cell line STC-1 expresses functional GABAA receptors and that GABA stimulates CCK release. Thus, GABA is involved in the fine tuning of CCK secretion from the gut NE cell line STC-1.

Indexed as

AnimalsCalciumCell LineChloride ChannelsCholecystokininElectric StimulationElectrophysiologygamma-Aminobutyric AcidIon Channel GatingMembrane PotentialsMiceNeurosecretory SystemsPatch-Clamp TechniquesPolymerase Chain ReactionReceptors, GABA-ARNA, MessengerCalciumChloride ChannelsCholecystokiningamma-Aminobutyric AcidReceptors, GABA-ARNA, Messenger

Identifiers

PMID9660895
PMCPMC2231074
OpenAlexW2013746143

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.