Evidence map›Paper›PMID 29077837›Full record

ArticleEndocrinology2018

Selective Pharmacogenetic Activation of Catecholamine Subgroups in the Ventrolateral Medulla Elicits Key Glucoregulatory Responses.

Ai-Jun Li, Qing Wang, Sue Ritter

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Endocrinology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

34 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  8. CCK-sensitive C fibers activate NTS leptin receptor-expressing neurons via NMDA receptors.American journal of physiology. Regulatory, integrative and comparative physiology · 2024
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  15. Chemogenetic activation of ventral medullary astrocytes enhances feeding and corticosterone release in response to mild glucoprivation.American journal of physiology. Regulatory, integrative and comparative physiology · 2023
    Article
  16. Article
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  18. Review
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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 1 institution in 1 country.

Ai-Jun LiPrograms in Neuroscience, Washington State University, Pullman, Washington.
Qing WangPrograms in Neuroscience, Washington State University, Pullman, Washington.
Sue RitterPrograms in Neuroscience, Washington State University, Pullman, Washington.
Washington State University · US

Funding

WNK Kinase Regulation of Thiazide-sensitive NaCl TransportR01DK051496 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI David Hoadley Ellison, CHAO-LING YANG · 1998 to 2026
$8.4M
NEURAL SUBSTRATES OF METABOLIC CONTROLS OF INGESTIONR01DK040498 · NIDDK · WASHINGTON STATE UNIVERSITY · PI RITTER, W. SUE · 1989 to 2014
$4.3M
Mechanisms of Fatty Acid Control of Feeding BehaviorR01DK097437 · NIDDK · WASHINGTON STATE UNIVERSITY · PI RITTER, W. SUE · 2013 to 2016
$1.3M
NIDDK NIH HHS R01 DK040498NIDDK NIH HHS R01 DK051496NIDDK NIH HHS R01 DK097437
6 · The paper itself

Abstract

Catecholamine (CA) neurons in the ventrolateral medulla (VLM) contribute importantly to glucoregulation during glucose deficit. However, it is not known which CA neurons elicit different glucoregulatory responses or whether selective activation of CA neurons is sufficient to elicit these responses. Therefore, to selectively activate CA subpopulations, we injected male or female Th-Cre+ transgenic rats with the Cre-dependent DREADD construct, AAV2-DIO-hSyn-hM3D(Gq)-mCherry, at one of four rostrocaudal levels of the VLM: rostral C1 (C1r), middle C1 (C1m), the area of A1 and C1 overlap (A1/C1), and A1. Transfection was highly selective for CA neurons at each site. Systemic injection of the Designer Receptor Exclusively Activated by Designer Drugs (DREADD) receptor agonist, clozapine-N-oxide (CNO), stimulated feeding in rats transfected at C1r, C1m, or A1/C1 but not A1. CNO increased corticosterone secretion in rats transfected at C1m or A1/C1 but not A1. In contrast, CNO did not increase blood glucose or induce c-Fos expression in the spinal cord or adrenal medulla after transfection of any single VLM site but required dual transfection of both C1m and C1r, possibly indicating that CA neurons mediating blood glucose responses are more sparsely distributed in C1r and C1m than those mediating feeding and corticosterone secretion. These results show that selective activation of C1 CA neurons is sufficient to increase feeding, blood glucose levels, and corticosterone secretion and suggest that each of these responses is mediated by CA neurons concentrated at different levels of the C1 cell group.

Indexed as

Pharmacogenomic VariantsActivation, MetabolicAdrenal MedullaAnimalsAntipsychotic AgentsBehavior, AnimalCatecholaminesClozapineFeeding BehaviorFemaleHumansHyperglycemiaLuminescent ProteinsMaleMedulla OblongataNerve Tissue ProteinsAntipsychotic AgentsCatecholaminesClozapineclozapine N-oxideLuminescent ProteinsNerve Tissue ProteinsReceptors, DrugRecombinant Fusion ProteinsRed Fluorescent Protein

Identifiers

PMID29077837
PMCPMC5761588
OpenAlexW2766340254

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.