Evidence map›Paper›PMID 26350161›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2015

Interaction of CRF and kappa opioid systems on GABAergic neurotransmission in the mouse central amygdala.

Maenghee Kang-Park, Brigitte L Kieffer, Amanda J Roberts, George R Siggins, Scott D Moore

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed, 40 citations in OpenAlex.

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  16. Article
  17. The amygdalar opioid system.Handbook of behavioral neuroscience · 2020
    Article
  18. Review
  19. Dynorphin-kappa opioid receptor activity in the central amygdala modulates binge-like alcohol drinking in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019
    Article
  20. 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

5 authors at 5 institutions in 3 countries.

Maenghee Kang-ParkDepartment of Psychiatry, Duke University Medical Center, and Research Service, Veterans Administration Medical Center, Durham, North Carolina (M.K., S.D.M.); IGBMC, CNRS/INSERM/ULP, Strasbourg, France, and McGill, Douglas Institute Research Center, Montréal, Canada (B.L.K.); Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, and Alcohol Research Center, La Jolla, California (A.J.R., G.R.S.).
Brigitte L KiefferDepartment of Psychiatry, Duke University Medical Center, and Research Service, Veterans Administration Medical Center, Durham, North Carolina (M.K., S.D.M.); IGBMC, CNRS/INSERM/ULP, Strasbourg, France, and McGill, Douglas Institute Research Center, Montréal, Canada (B.L.K.); Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, and Alcohol Research Center, La Jolla, California (A.J.R., G.R.S.).
Amanda J RobertsDepartment of Psychiatry, Duke University Medical Center, and Research Service, Veterans Administration Medical Center, Durham, North Carolina (M.K., S.D.M.); IGBMC, CNRS/INSERM/ULP, Strasbourg, France, and McGill, Douglas Institute Research Center, Montréal, Canada (B.L.K.); Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, and Alcohol Research Center, La Jolla, California (A.J.R., G.R.S.).
George R SigginsDepartment of Psychiatry, Duke University Medical Center, and Research Service, Veterans Administration Medical Center, Durham, North Carolina (M.K., S.D.M.); IGBMC, CNRS/INSERM/ULP, Strasbourg, France, and McGill, Douglas Institute Research Center, Montréal, Canada (B.L.K.); Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, and Alcohol Research Center, La Jolla, California (A.J.R., G.R.S.).
Scott D MooreDepartment of Psychiatry, Duke University Medical Center, and Research Service, Veterans Administration Medical Center, Durham, North Carolina (M.K., S.D.M.); IGBMC, CNRS/INSERM/ULP, Strasbourg, France, and McGill, Douglas Institute Research Center, Montréal, Canada (B.L.K.); Department of Molecular and Cellular Neuroscience, The Scripps Research Institute, and Alcohol Research Center, La Jolla, California (A.J.R., G.R.S.) sdmoore@duke.edu.
Centre National de la Recherche Scientifique · FRDouglas Mental Health University Institute · CADuke University Hospital · USInserm · FRInstitut de génétique et de biologie moléculaire et cellulaire · FR

Funding

Electrophysiology of alcohol in extended amygdelaU01AA013498 · NIAAA · SCRIPPS RESEARCH INSTITUTE, THE · PI MARISA ROBERTO · 2001 to 2026
$12.6M
Nr4a1 and GPR88 as novel gene targets for alcoholism: mouse genetic approachesU01AA016658 · NIAAA · UNIVERSITE DE STRASBOURG · PI LAURA ADELA HARSAN · 2006 to 2026
$3.8M
MORPHINE-LIKE BRAIN PEPTIDES: CELLULAR NEUROBIOLOGYR01DA003665 · NIDA · SCRIPPS RESEARCH INSTITUTE, THE · PI SIGGINS, GEORGE ROBERT · 1985 to 2008
$2.2M
Mechanisms underlying neuropeptide release in the extended amygdalaI01BX001271 · VA · DURHAM VA MEDICAL CENTER · PI MOORE, SCOTT D. · 2013 to 2020
–
BLRD VA I01 BX001271NIAAA NIH HHS AA16658NIAAA NIH HHS U01 AA013498NIAAA NIH HHS U01 AA016658NIDA NIH HHS R01 DA003665NIDA NIH HHS R01 DA03665
6 · The paper itself

Abstract

The corticotropin-releasing factor (CRF) and kappa-opioid receptor (KOR) systems are both implicated in stress-related behaviors and drug dependence. Although previous studies suggest that antagonism of each system blocks aspects of experimental models of drug dependence, the possible interaction between these systems at the neuronal level has not been completely examined. We used an in vitro brain slice preparation to investigate the interaction of these two peptide systems on inhibitory neurotransmission in the central nucleus of the amygdala (CeA). Application of exogenous CRF increased the mean frequency of GABAergic miniature inhibitory postsynaptic currents (mIPSC) by 20.2%, suggesting an increase in presynaptic GABA release. Although the pharmacological blockade of KORs by norBNI alone did not significantly affect mIPSC frequency, it significantly enhanced the effect of CRF (by 43.9%, P = 0.02). Similarly, the CRF effects in slices from KOR knockout (KO) mice (84.0% increase) were significantly greater than in wild-type (WT) mice (24.6%, P = 0.01), although there was no significant difference in baseline mIPSC frequency between slices from KOR KO and WT mice. The increase in CRF action in the presence of norBNI was abolished by a CRF-1 receptor antagonist but was unaffected by a CRF-2 receptor antagonist. We hypothesize that CRF facilitates the release of an endogenous ligand for KORs and that subsequent activation of KOR receptors modulates presynaptic effects of CRF in CeA. These results suggest that potential pharmacotherapies aimed at neurobehavioral and addictive disorders may need to involve both the KOR/dynorphin and the CRF systems in CeA.

Indexed as

AnimalsCentral Amygdaloid NucleusCorticotropin-Releasing HormoneCRF Receptor, Type 1gamma-Aminobutyric AcidInhibitory Postsynaptic PotentialsMice, Inbred C57BLMice, KnockoutMiniature Postsynaptic PotentialsNaltrexoneReceptors, Corticotropin-Releasing HormoneReceptors, Opioid, kappaSynaptic TransmissionCorticotropin-Releasing HormoneCRF Receptor, Type 1CRF receptor type 2gamma-Aminobutyric AcidNaltrexonenorbinaltorphimineReceptors, Corticotropin-Releasing HormoneReceptors, Opioid, kappa

Identifiers

PMID26350161
PMCPMC4613963
OpenAlexW1650998670

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.