Evidence map›Paper›PMID 26733798›Full record

ArticleFrontiers in neuroscience2015

A Transgenic Rat for Investigating the Anatomy and Function of Corticotrophin Releasing Factor Circuits.

Matthew B Pomrenze, E Zayra Millan, F Woodward Hopf, Ronald Keiflin, Rajani Maiya, Angelo Blasio, Jahan Dadgar, Viktor Kharazia, Giordano De Guglielmo, Elena Crawford and 4 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

91 citing papers in PubMed, 136 citations in OpenAlex.

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  16. A pharynx-to-brain axis controls pharyngeal inflammation-induced anxiety.Proceedings of the National Academy of Sciences of the United States of America · 2024
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31 more citing papers are in PubMed but not listed here.

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

14 authors at 4 institutions in 1 country.

Matthew B PomrenzeDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin Austin, TX, USA.
E Zayra MillanDepartment of Neurology, University of California, San Francisco San Francisco, CA, USA.
F Woodward HopfDepartment of Neurology, University of California, San Francisco San Francisco, CA, USA.
Ronald KeiflinDepartment of Neurology, University of California, San Francisco San Francisco, CA, USA.
Rajani MaiyaDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin Austin, TX, USA.
Angelo BlasioDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin Austin, TX, USA.
Jahan DadgarDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at AustinAustin, TX, USA; Department of Neurology, University of California, San FranciscoSan Francisco, CA, USA.
Viktor KharaziaDepartment of Neurology, University of California, San Francisco San Francisco, CA, USA.
Giordano De GuglielmoCommittee on The Neurobiology of Addictive Disorders, The Scripps Research Institute La Jolla, CA, USA.
Elena CrawfordCommittee on The Neurobiology of Addictive Disorders, The Scripps Research Institute La Jolla, CA, USA.
Patricia H JanakDepartment of Neurology, University of California, San Francisco San Francisco, CA, USA.
Olivier GeorgeCommittee on The Neurobiology of Addictive Disorders, The Scripps Research Institute La Jolla, CA, USA.
Kenner C RiceChemical Biology Research Branch, Drug Design and Synthesis Section, National Institute on Drug Abuse, National Institute on Alcohol Abuse and Alcoholism Rockville, MD, USA.
Robert O MessingDivision of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at AustinAustin, TX, USA; Department of Neurology, University of California, San FranciscoSan Francisco, CA, USA.
University of California, San Francisco · USScripps Research Institute · USThe University of Texas at Austin · USNational Institute on Drug Abuse · US

Funding

Vector, Transgenic, and Imaging CoreP50AA017072 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI RON, DORIT · 2008 to 2017
$13.9M
Alcohol Vapor Self-Administration in RatsR01AA022977 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Olivier George · 2014 to 2026
$5.1M
Regulation of GABAA Receptors by PKC epsilon.R01AA013588 · NIAAA · UNIVERSITY OF TEXAS AT AUSTIN · PI MESSING, ROBERT O. · 2002 to 2016
$1.9M
Medicinal Chemistry of Drugs Acting on CRH ReceptorsZIADA000528 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI RICE, KENNER · 2009 to 2018
$1.8M
Opto/Chemo-genetic Analysis of Locus Coeruleus CRF and Compulsive Ethanol IntakeR21AA023223 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HOPF, FREDERIC WOODWARD · 2015 to 2016
$430k
NIAAA NIH HHS P50 AA017072NIAAA NIH HHS R01 AA013588NIAAA NIH HHS R01 AA022977NIAAA NIH HHS R21 AA023223
6 · The paper itself

Abstract

Corticotrophin-releasing factor (CRF) is a 41 amino acid neuropeptide that coordinates adaptive responses to stress. CRF projections from neurons in the central nucleus of the amygdala (CeA) to the brainstem are of particular interest for their role in motivated behavior. To directly examine the anatomy and function of CRF neurons, we generated a BAC transgenic Crh-Cre rat in which bacterial Cre recombinase is expressed from the Crh promoter. Using Cre-dependent reporters, we found that Cre expressing neurons in these rats are immunoreactive for CRF and are clustered in the lateral CeA (CeL) and the oval nucleus of the BNST. We detected major projections from CeA CRF neurons to parabrachial nuclei and the locus coeruleus, dorsal and ventral BNST, and more minor projections to lateral portions of the substantia nigra, ventral tegmental area, and lateral hypothalamus. Optogenetic stimulation of CeA CRF neurons evoked GABA-ergic responses in 11% of non-CRF neurons in the medial CeA (CeM) and 44% of non-CRF neurons in the CeL. Chemogenetic stimulation of CeA CRF neurons induced Fos in a similar proportion of non-CRF CeM neurons but a smaller proportion of non-CRF CeL neurons. The CRF1 receptor antagonist R121919 reduced this Fos induction by two-thirds in these regions. These results indicate that CeL CRF neurons provide both local inhibitory GABA and excitatory CRF signals to other CeA neurons, and demonstrate the value of the Crh-Cre rat as a tool for studying circuit function and physiology of CRF neurons.

Indexed as

central amygdalachannelrhodopsin-2Cre recombinaseCRFdesigner receptors exclusively activated by designer drugsFosR121919transgenic rat models

Identifiers

PMID26733798
PMCPMC4689854
OpenAlexW2232850269

What OpenQuestion holds

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Registered trials

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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.