Evidence map›Paper›PMID 36114285›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2023

Nucleus of the solitary tract A2 neurons control feeding behaviors via projections to the paraventricular hypothalamus.

Stephanie Murphy, Metika Collis Glynn, Tiarani N Dixon, Harvey J Grill, Gavan P McNally, Zhi Yi Ong

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

  1. Trial
  2. 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
  3. Article
  4. The critical role of gut-brain signalling in eating behaviour and obesity.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  5. Article
  6. Article
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  19. Stress integration by an ascending adrenergic-melanocortin circuit.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    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 2 institutions in 2 countries.

Stephanie Murphy *School of Psychology, University of New South Wales, UNSW, Sydney, NSW, 2052, Australia.
Metika Collis Glynn *School of Psychology, University of New South Wales, UNSW, Sydney, NSW, 2052, Australia.
Tiarani N DixonSchool of Psychology, University of New South Wales, UNSW, Sydney, NSW, 2052, Australia.
Harvey J GrillDepartment of Psychology, Institute of Diabetes Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA, 19104, USA.
Gavan P McNallySchool of Psychology, University of New South Wales, UNSW, Sydney, NSW, 2052, Australia.ORCID 0000-0001-9061-6463
Zhi Yi OngSchool of Psychology, University of New South Wales, UNSW, Sydney, NSW, 2052, Australia. zhiyi.ong@unsw.edu.au.ORCID 0000-0002-8300-6955
UNSW Sydney · AUUniversity of Pennsylvania · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hindbrain NTS neurons are highly attuned to internal physiological and external environmental factors that contribute to the control of food intake but the relevant neural phenotypes and pathways remain elusive. Here, we investigated the role of NTS A2 neurons and their projections in the control of feeding behaviors. In male TH Cre rats, we first confirmed selective targeting of NTS A2 neurons and showed that chemogenetic stimulation of these neurons significantly suppressed dark cycle food intake, deprivation re-feed and high fat diet intake. Despite reducing intake, activation of NTS A2 neurons had no effect on food approach, anxiety-like behaviors, locomotor activity, blood glucose levels nor did it induce nausea/malaise, thus revealing a selective role for these neurons in the consummatory aspect of food intake control. Pathway-specific mapping and manipulation of NTS A2 neurons showed that these effects were mediated by NTS A2 neurons projecting to the paraventricular nucleus of the hypothalamus (PVH) because chemogenetic activation of these projections, but not projections to bed nucleus of the stria terminalis (BNST), reduced food intake. Cell-type specific analyses demonstrated that activation of NTS A2 neurons recruited both PVH oxytocin (OT)- and corticotropin-releasing factor (CRF)-expressing neurons, and plasma analyses showed increased plasma corticosterone following NTS A2 stimulation. While we also showed that chemogenetic inhibition of NTS A2 neurons attenuated the intake inhibitory effects of CCK, the specificity of transgene expression was low. Together, these findings showed that NTS A2 neurons are sufficient to control the consummatory aspects of feeding, regardless of energy status or food palatability and identified their projections to PVH, but not BNST, in food intake control.

Indexed as

HypothalamusSolitary NucleusAnimalsFeeding BehaviorMaleNeuronsParaventricular Hypothalamic NucleusRats

Identifiers

PMID36114285
PMCPMC9751294
OpenAlexW4296163822

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.