Evidence map›Paper›PMID 22171049›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

MAP kinases couple hindbrain-derived catecholamine signals to hypothalamic adrenocortical control mechanisms during glycemia-related challenges.

Arshad M Khan, Kimberly L Kaminski, Graciela Sanchez-Watts, Todd A Ponzio, J Brent Kuzmiski, Jaideep S Bains, Alan G Watts

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. 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
1.5field-weighted citation impact, top 22% 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, 40 citations in OpenAlex.

  1. Review
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  11. Catecholaminergic projections into an interconnected forebrain network control the sensitivity of male rats to diet-induced obesity.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
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  12. Article
  13. Review
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  15. Rapid-onset hypoglycemia suppresses Fos expression in discrete parts of the ventromedial nucleus of the hypothalamus.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  16. Article
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  20. Stimulation of feeding by three different glucose-sensing mechanisms requires hindbrain catecholamine neurons.American journal of physiology. Regulatory, integrative and comparative physiology · 2014
    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

7 authors at 3 institutions in 2 countries.

Arshad M KhanDepartment of Biological Sciences, University of Southern California, Los Angeles, California 90089, USA. amkhan2@utep.edu
Kimberly L Kaminski
Graciela Sanchez-Watts
Todd A Ponzio
J Brent Kuzmiski
Jaideep S Bains
Alan G Watts
University of Southern California · USUniversity of Calgary · CANational Institutes of Health · US

Funding

NEUROPEPTIDES AND THEIR PHYSIOLOGICAL CONTROLR01NS029728 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI WATTS, ALAN G · 1991 to 2017
$4.5M
From glucosensing neurons to CRH neuroedocrine neurons: Circuits and signalsK01DK081937 · NIDDK · UNIVERSITY OF TEXAS EL PASO · PI KHAN, ARSHAD M. · 2008 to 2011
$515k
Signal Transduction Mechanisms in Neuroendocrine NeuronsF32MH071108 · NIMH · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KHAN, ARSHAD M · 2004 to 2006
$149k
CIHRNIDDK NIH HHS DK081937NIDDK NIH HHS K01 DK081937NIMH NIH HHS F32 MH071108NIMH NIH HHS MH071108NINDS NIH HHS NS029728NINDS NIH HHS R01 NS029728
6 · The paper itself

Abstract

Physiological responses to hypoglycemia, hyperinsulinemia, and hyperglycemia include a critical adrenocortical component that is initiated by hypothalamic control of the anterior pituitary and adrenal cortex. These adrenocortical responses ensure appropriate long-term glucocorticoid-mediated modifications to metabolism. Despite the importance of these mechanisms to disease processes, how hypothalamic afferent pathways engage the intracellular mechanisms that initiate adrenocortical responses to glycemia-related challenges are unknown. This study explores these mechanisms using network- and cellular-level interventions in in vivo and ex vivo rat preparations. Results show that a hindbrain-originating catecholamine afferent system selectively engages a MAP kinase pathway in rat paraventricular hypothalamic CRH (corticotropin-releasing hormone) neuroendocrine neurons shortly after vascular insulin and 2-deoxyglucose challenges. In turn, this MAP kinase pathway can control both neuroendocrine neuronal firing rate and the state of CREB phosphorylation in a reduced ex vivo paraventricular hypothalamic preparation, making this signaling pathway an ideal candidate for coordinating CRH synthesis and release. These results establish the first clear structural and functional relationships linking neurons in known nutrient-sensing regions with intracellular mechanisms in hypothalamic CRH neuroendocrine neurons that initiate the adrenocortical response to various glycemia-related challenges.

Indexed as

AnimalsBlood GlucoseCatecholaminesDeoxyglucoseHypothalamo-Hypophyseal SystemHypothalamusInsulinMaleMAP Kinase Signaling SystemNeuronsPhosphorylationPituitary-Adrenal SystemRatsRats, Sprague-DawleyRhombencephalonBlood GlucoseCatecholaminesDeoxyglucoseInsulin

Identifiers

PMID22171049
PMCPMC3293627
OpenAlexW2009047934

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.