Evidence map›Paper›PMID 25595987›Full record

ArticleNeuroscience2015

Neuroanatomical and functional characterization of CRF neurons of the amygdala using a novel transgenic mouse model.

P N De Francesco, S Valdivia, A Cabral, M Reynaldo, J Raingo, I Sakata, S Osborne-Lawrence, J M Zigman, M Perelló

Open access · bronzeAbstract read
In one paragraph

Article in Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.8field-weighted citation impact, top 18% 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

17 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  4. Neuroendocrine control of appetite and metabolism.Experimental & molecular medicine · 2021
    Review
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  6. Secretagogin marks amygdaloid PKCδ interneurons and modulates NMDA receptor availability.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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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

9 authors at 2 institutions in 2 countries.

P N De FrancescoLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina.
S ValdiviaLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina.
A CabralLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina.
M ReynaldoLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina.
J RaingoLaboratory of Electrophysiology, Multidisciplinary Institute of Cell Biology [Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina.
I SakataDivision of Hypothalamic Research and Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States; Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, United States.
S Osborne-LawrenceDivision of Hypothalamic Research and Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States; Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, United States.
J M ZigmanDivision of Hypothalamic Research and Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, United States; Department of Psychiatry, University of Texas Southwestern Medical Center, Dallas, TX, United States.
M PerellóLaboratory of Neurophysiology, Multidisciplinary Institute of Cell Biology [Argentine Research Council (CONICET) and Scientific Research Commission, Province of Buenos Aires (CIC-PBA)], La Plata, Buenos Aires, Argentina. Electronic address: marioperello@yahoo.com.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARThe University of Texas Southwestern Medical Center · US

Funding

Ghrelin's Role in MoodR01MH085298 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI ZIGMAN, JEFFREY M · 2010 to 2014
$2.0M
Role of the Central Amygdala in Ghrelin-Mediated Reward-Based Eating BehaviorR03TW008925 · FIC · UT SOUTHWESTERN MEDICAL CENTER · PI ZIGMAN, JEFFREY M · 2012 to 2013
$121k
FIC NIH HHS R03 TW008925FIC NIH HHS R03TW008925-01A1NIMH NIH HHS R01 MH085298NIMH NIH HHS R01MH085298
6 · The paper itself

Abstract

The corticotropin-releasing factor (CRF)-producing neurons of the amygdala have been implicated in behavioral and physiological responses associated with fear, anxiety, stress, food intake and reward. To overcome the difficulties in identifying CRF neurons within the amygdala, a novel transgenic mouse line, in which the humanized recombinant Renilla reniformis green fluorescent protein (hrGFP) is under the control of the CRF promoter (CRF-hrGFP mice), was developed. First, the CRF-hrGFP mouse model was validated and the localization of CRF neurons within the amygdala was systematically mapped. Amygdalar hrGFP-expressing neurons were located primarily in the interstitial nucleus of the posterior limb of the anterior commissure, but also present in the central amygdala. Secondly, the marker of neuronal activation c-Fos was used to explore the response of amygdalar CRF neurons in CRF-hrGFP mice under different experimental paradigms. C-Fos induction was observed in CRF neurons of CRF-hrGFP mice exposed to an acute social defeat stress event, a fasting/refeeding paradigm or lipopolysaccharide (LPS) administration. In contrast, no c-Fos induction was detected in CRF neurons of CRF-hrGFP mice exposed to restraint stress, forced swimming test, 48-h fasting, acute high-fat diet (HFD) consumption, intermittent HFD consumption, ad libitum HFD consumption, HFD withdrawal, conditioned HFD aversion, ghrelin administration or melanocortin 4 receptor agonist administration. Thus, this study fully characterizes the distribution of amygdala CRF neurons in mice and suggests that they are involved in some, but not all, stress or food intake-related behaviors recruiting the amygdala.

Indexed as

Amphibian ProteinsAmygdalaAnimalsCorticotropin-Releasing HormoneDiet, High-FatDominance-SubordinationEatingFastingGhrelinGreen Fluorescent ProteinsLipopolysaccharidesMaleMice, Inbred C57BLMice, TransgenicNeuronsProto-Oncogene Proteins c-fosAmphibian ProteinsCorticotropin-Releasing HormoneGhrelinGreen Fluorescent ProteinsLipopolysaccharidesMC4R protein, mouseProto-Oncogene Proteins c-fosReceptor, Melanocortin, Type 4Recombinant ProteinsamygdalaCRHfood intakestress

Identifiers

PMID25595987
PMCPMC4344851
OpenAlexW1964627324

What OpenQuestion holds

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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.