Evidence map›Paper›PMID 22508518›Full record

ArticleEndocrinology2012

CCK-induced reduction of food intake and hindbrain MAPK signaling are mediated by NMDA receptor activation.

Carlos A Campos, Jason S Wright, Krzysztof Czaja, Robert C Ritter

Open access · bronzeAbstract read
In one paragraph

Article in Endocrinology, 2012. 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
1.8field-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, 48 citations in OpenAlex.

  1. Article
  2. CCK-sensitive C fibers activate NTS leptin receptor-expressing neurons via NMDA receptors.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Optogenetic Manipulation of the Vagus Nerve.Advances in experimental medicine and biology · 2021
    Article
  10. Article
  11. Leptin Sensitizes NTS Neurons to Vagal Input by Increasing Postsynaptic NMDA Receptor Currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Melanocortin neurons: Multiple routes to regulation of metabolism.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Review
  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

4 authors at 1 institution in 1 country.

Carlos A CamposDepartment of Veterinary and Comparative Anatomy, Pharmacology, and Physiology and Programs in Neuroscience, College of Veterinary Medicine, Washington State University, Pullman, Washington 99164-6520, USA.
Jason S Wright
Krzysztof Czaja
Robert C Ritter
Washington State University · US

Funding

The Role of Glutamate in the Control of Food IntakeR01DK052849 · NIDDK · WASHINGTON STATE UNIVERSITY · PI APPLEYARD, SUZANNE M, RITTER, ROBERT C · 1998 to 2021
$6.3M
NEURAL SUBSTRATES OF PEPTIDE-INDUCED SATIETYR01NS020561 · NINDS · WASHINGTON STATE UNIVERSITY · PI RITTER, ROBERT C · 1985 to 2012
$3.6M
NIDDK NIH HHS DK-52849NIDDK NIH HHS R01 DK052849NINDS NIH HHS NS-20561NINDS NIH HHS R01 NS020561
6 · The paper itself

Abstract

The dorsal vagal complex of the hindbrain, including the nucleus of the solitary tract (NTS), receives neural and humoral afferents that contribute to the process of satiation. The gut peptide, cholecystokinin (CCK), promotes satiation by activating gastrointestinal vagal afferents that synapse in the NTS. Previously, we demonstrated that hindbrain administration of N-methyl-D-aspartate (NMDA)-type glutamate receptor antagonists attenuate reduction of food intake after ip CCK-8 injection, indicating that these receptors play a necessary role in control of food intake by CCK. However, the signaling pathways through which hindbrain NMDA receptors contribute to CCK-induced reduction of food intake have not been investigated. Here we report CCK increases phospho-ERK1/2 in NTS neurons and in identified vagal afferent endings in the NTS. CCK-evoked phospho-ERK1/2 in the NTS was attenuated in rats pretreated with capsaicin and was abolished by systemic injection of a CCK1 receptor antagonist, indicating that phosphorylation of ERK1/2 occurs in and is mediated by gastrointestinal vagal afferents. Fourth ventricle injection of a competitive NMDA receptor antagonist, prevented CCK-induced phosphorylation of ERK1/2 in hindbrain neurons and in vagal afferent endings, as did direct inhibition of MAPK kinase. Finally, fourth ventricle administration of either a MAPK kinase inhibitor or NMDA receptor antagonist prevented the reduction of food intake by CCK. We conclude that activation of NMDA receptors in the hindbrain is necessary for CCK-induced ERK1/2 phosphorylation in the NTS and consequent reduction of food intake.

Indexed as

AnimalsButadienesCholecystokininDevazepideEatingEnzyme InhibitorsExcitatory Amino Acid AntagonistsHormone AntagonistsImmunohistochemistryMaleMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NeuronsNitrilesPhosphorylationButadienesCholecystokininDevazepideEnzyme InhibitorsExcitatory Amino Acid AntagonistsHormone AntagonistsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3NitrilesPiperazinesReceptors, CholecystokininReceptors, N-Methyl-D-AspartateSDZ EAA 494U 0126

Identifiers

PMID22508518
PMCPMC3359610
OpenAlexW2116826007

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.