Evidence map›Paper›PMID 18655818›Full record

ArticlePeptides2008

Mechanisms of action of CCK to activate central vagal afferent terminals.

Richard C Rogers, Gerlinda E Hermann

Open access · greenAbstract read
In one paragraph

Article in Peptides, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.9field-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

28 citing papers in PubMed, 55 citations in OpenAlex.

  1. Cholecystokinin Induces CaThe European journal of neuroscience · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Role of the gut-brain axis in energy and glucose metabolism.Experimental & molecular medicine · 2022
    Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Plasticity of vagal afferent signaling in the gut.Medicina (Kaunas, Lithuania) · 2017
    Review
  17. Article
  18. Incretin hormones and the satiation signal.International journal of obesity (2005) · 2013
    Review
  19. Article
  20. Tumor necrosis factor activation of vagal afferent terminal calcium is blocked by cannabinoids.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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 1 country.

Richard C RogersLaboratory of Autonomic Neurosciences, Pennington Biomedical Research Center, Baton Rouge, LA 70808, USA. Richard.Rogers@pbrc.edu
Gerlinda E Hermann
Pennington Biomedical Research Center · USRogers (United States) · US

Funding

TNF, VAGAL TONE AND GASTRIC MOTILITYR01DK052142 · NIDDK · OHIO STATE UNIVERSITY · PI ROGERS, RICHARD C. · 1997 to 2013
$3.1M
Brainstem Esophageal-Gastric ReflexesR01DK056373 · NIDDK · OHIO STATE UNIVERSITY · PI ROGERS, RICHARD C. · 1999 to 2009
$2.1M
Thrombin and CNS: Gastric Dysfunction after Head TraumaR21HD047643 · NICHD · LSU PENNINGTON BIOMEDICAL RESEARCH CTR · PI HERMANN, GERLINDA E · 2005 to 2006
$257k
NICHD NIH HHS HD 47643NICHD NIH HHS R21 HD047643NIDDK NIH HHS DK 52142NIDDK NIH HHS DK56373NIDDK NIH HHS R01 DK052142NIDDK NIH HHS R01 DK056373
6 · The paper itself

Abstract

Cholecystokinin [CCK] is a peptide released as a hormone by the proximal gut in response to the presence of peptones and fatty acid in the gut. Considerable evidence suggests that CCK inhibits feeding behavior and gastric function by acting as a paracrine modulator of vagal afferents in the periphery, especially in the duodenum. CCK is also widely distributed throughout the mammalian brain and appears to function as a neurotransmitter and neuromodulator. More recent studies have suggested that CCK may act directly within the CNS to activate central vagal afferent terminal inputs to the solitary nucleus. We have developed an in vitro calcium imaging method that reveals, for the first time, the direct effects of this peptide on vagal terminals in the solitary nucleus. In vitro imaging reveals that CCK provokes increases in intracellular calcium in vagal afferent terminals as a consequence of a complex interaction between protein kinase A [PKA] and phospholipase C [PLC] transduction mechanisms that open L-type calcium channels and causes endoplasmic reticular [ER] calcium release. The subsequent activation of PKC may be responsible for initiating calcium spiking which is dependent on a TTX-sensitive mechanism. Thus, imaging of the isolated but spatially intact hindbrain slice has allowed a more complete appreciation of the interdependent transduction mechanisms used by CCK to excite identified central vagal afferent fibers and varicosities.

Indexed as

Afferent PathwaysAnimalsCalciumCalcium Channel BlockersCholecystokininElectrophysiologyEnzyme InhibitorsFemaleMalePresynaptic TerminalsRatsRats, Long-EvansSignal TransductionVagus NerveCalciumCalcium Channel BlockersCholecystokininEnzyme Inhibitors

Identifiers

PMID18655818
PMCPMC2650377
OpenAlexW2022917608

What OpenQuestion holds

Textmetadata
LicenceTDM
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.