Evidence map›Paper›PMID 15564576›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

Lateral hypothalamic signaling mechanisms underlying feeding stimulation: differential contributions of Src family tyrosine kinases to feeding triggered either by NMDA injection or by food deprivation.

Arshad M Khan, Herman H Cheung, Elizabeth R Gillard, Jennifer A Palarca, Derek S Welsbie, James W Gurd, B Glenn Stanley

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.5field-weighted citation impact, top 46% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
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  5. Review
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  8. Antagonism of glutamatergic NMDA and mGluR5 receptors decreases consumption of food in baboon model of binge-eating disorder.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2008
    Article
  9. Article
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  12. Review
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 4 institutions in 3 countries.

Arshad M KhanDepartment of Cell Biology and Neuroscience, University of California, Riverside, California 92521, USA. arshadk@usc.edu
Herman H Cheung
Elizabeth R Gillard
Jennifer A Palarca
Derek S Welsbie
James W Gurd
B Glenn Stanley
Institute of Cell Biology and Neurobiology · ITUniversity of California, Riverside · USUniversity of Toronto · CASouthern California University for Professional Studies · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In rats, feeding can be triggered experimentally using many approaches. Included among these are (1) food deprivation and (2) acute microinjection of the neurotransmitter l-glutamate (Glu) or its receptor agonist NMDA into the lateral hypothalamic area (LHA). Under both paradigms, the NMDA receptor (NMDA-R) within the LHA appears critically involved in transferring signals encoded by Glu to stimulate feeding. However, the intracellular mechanisms underlying this signal transfer are unknown. Because protein-tyrosine kinases (PTKs) participate in NMDA-R signaling mechanisms, we determined PTK involvement in LHA mechanisms underlying both types of feeding stimulation through food intake and biochemical measurements. LHA injections of PTK inhibitors significantly suppressed feeding elicited by LHA NMDA injection (up to 69%) but only mildly suppressed deprivation feeding (24%), suggesting that PTKs may be less critical for signals underlying this feeding behavior. Conversely, food deprivation but not NMDA injection produced marked increases in apparent activity for Src PTKs and in the expression of Pyk2, an Src-activating PTK. When considered together, the behavioral and biochemical results demonstrate that, although it is easier to suppress NMDA-elicited feeding by PTK inhibitors, food deprivation readily drives PTK activity in vivo. The latter result may reflect greater PTK recruitment by neurotransmitter receptors, distinct from the NMDA-R, that are activated during deprivation-elicited but not NMDA-elicited feeding. These results also demonstrate how the use of only one feeding stimulation paradigm may fail to reveal the true contributions of signaling molecules to pathways underlying feeding behavior in vivo.

Indexed as

AnimalsBlotting, WesternButadienesFeeding BehaviorFocal Adhesion Kinase 2Food DeprivationGenisteinHypothalamic Area, LateralImmunoenzyme TechniquesImmunoprecipitationKainic AcidMaleNitrilesN-MethylaspartatePhosphorylationProtein-Tyrosine Kinases2-amino-4-(4'-hydroxyphenyl)-1,1,3-tricyanobuta-1,3-diene4-amino-5-(4-methylphenyl)-7-(tert-butyl)pyrazolo(3,4-d)pyrimidineButadienesFocal Adhesion Kinase 2GenisteinKainic AcidNitrilesN-MethylaspartateProtein-Tyrosine KinasesPtk2b protein, ratPyrazolesPyrimidinesReceptors, N-Methyl-D-Aspartatesrc-Family Kinases

Identifiers

PMID15564576
PMCPMC6730118
OpenAlexW2014184957

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.