Evidence map›Paper›PMID 27301688›Full record

ArticleNature communications2016

Genetically and functionally defined NTS to PBN brain circuits mediating anorexia.

Carolyn W Roman, Victor A Derkach, Richard D Palmiter

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 173 papers.

0numbers the graph read from it
0cells of the map it votes in
173citing papers in PubMed
12.6field-weighted citation impact, top 1% 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

173 citing papers in PubMed, 296 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Nucleus of the solitary tract regulation of cue-induced appetitive behaviors via midbrain dopamine neurons.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  5. Article
  6. Article
  7. ParabrachialProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Parabrachial CGRP Neurons Regulate Opioid Reinforcement.bioRxiv : the preprint server for biology · 2026
    Article
  17. Cellular coding of ingestion in the caudal brainstem.bioRxiv : the preprint server for biology · 2026
    Article
  18. Review
  19. Review
  20. Article

113 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 1 country.

Carolyn W RomanDepartment of Biochemistry, University of Washington, Seattle, Washington 98195, USA.
Victor A DerkachDepartment of Biochemistry, University of Washington, Seattle, Washington 98195, USA.
Richard D PalmiterDepartment of Biochemistry, University of Washington, Seattle, Washington 98195, USA.
University of Washington · USHoward Hughes Medical Institute · US

Funding

Diabetes, Obesity and Metabolism Training ProgramT32DK007247 · NIDDK · UNIVERSITY OF WASHINGTON · PI GREGORY J MORTON, KRISTINA Marie UTZSCHNEIDER · 1986 to 2026
$10.0M
Effect of Killing or Removing GABA from NPY/AgRP NeuronsR01DA024908 · NIDA · UNIVERSITY OF WASHINGTON · PI PALMITER, RICHARD D. · 2007 to 2021
$3.5M
NIDA NIH HHS R01 DA024908NIDDK NIH HHS T32 DK007247
6 · The paper itself

Abstract

The central nervous system controls food consumption to maintain metabolic homoeostasis. In response to a meal, visceral signals from the gut activate neurons in the nucleus of the solitary tract (NTS) via the vagus nerve. These NTS neurons then excite brain regions known to mediate feeding behaviour, such as the lateral parabrachial nucleus (PBN). We previously described a neural circuit for appetite suppression involving calcitonin gene-related protein (CGRP)-expressing PBN (CGRP(PBN)) neurons; however, the molecular identity of the inputs to these neurons was not established. Here we identify cholecystokinin (CCK) and noradrenergic, dopamine β-hydroxylase (DBH)-expressing NTS neurons as two separate populations that directly excite CGRP(PBN) neurons. When these NTS neurons are activated using optogenetic or chemogenetic methods, food intake decreases and with chronic stimulation mice lose body weight. Our optogenetic results reveal that CCK and DBH neurons in the NTS directly engage CGRP(PBN) neurons to promote anorexia.

Indexed as

Action PotentialsAnimalsAnorexiaAnxietyCalcitonin Gene-Related PeptideCholecystokininDopamine beta-HydroxylaseEatingMice, Inbred C57BLNeural PathwaysNeuronsParabrachial NucleusProto-Oncogene Proteins c-fosSolitary NucleusCalcitonin Gene-Related PeptideCholecystokininDopamine beta-HydroxylaseProto-Oncogene Proteins c-fos

Identifiers

PMID27301688
PMCPMC4912612
OpenAlexW2439903663

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.