Evidence map›Paper›PMID 27044354›Full record

ArticlePsychopharmacology2016

The melanin-concentrating hormone-1 receptor modulates alcohol-induced reward and DARPP-32 phosphorylation.

Camilla Karlsson, Faazal Rehman, Ruslan Damadzic, Alison L Atkins, Jesse R Schank, Donald R Gehlert, Pia Steensland, Annika Thorsell, Markus Heilig

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

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  4. Regulation of the Mouse Ventral Tegmental Area by Melanin-Concentrating Hormone.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 6 institutions in 2 countries.

Camilla KarlssonDepartment of Clinical and Experimental Medicine, Linkopings University, Linkoping, Sweden.
Faazal RehmanLaboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), Bethesda, MD, USA.
Ruslan DamadzicLaboratory of Clinical and Translational Studies, National Institute on Alcohol Abuse and Alcoholism (NIAAA), National Institutes of Health (NIH), Bethesda, MD, USA.
Alison L AtkinsDepartment of Clinical and Experimental Medicine, Linkopings University, Linkoping, Sweden.
Jesse R SchankDepartment of Physiology and Pharmacology, University of Georgia, Athens, GA, USA.
Donald R GehlertNeuroscience and Endocrine Discovery Research, Lilly Research Laboratories, a Division of Eli Lilly and Company, Indianapolis, IN, USA.
Pia SteenslandDepartment of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
Annika ThorsellDepartment of Clinical and Experimental Medicine, Linkopings University, Linkoping, Sweden.
Markus HeiligDepartment of Clinical and Experimental Medicine, Linkopings University, Linkoping, Sweden. markus.heilig@liu.se.
Linköping University · SEEli Lilly (United States) · USKarolinska Institutet · SENational Institute on Alcohol Abuse and Alcoholism · USNational Institutes of Health · USUniversity of Georgia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleMelanin-concentrating hormone (MCH) is involved in the regulation of food intake and has recently been associated with alcohol-related behaviors. Blockade of MCH-1 receptors (MCH1-Rs) attenuates operant alcohol self-administration and decreases cue-induced reinstatement, but the mechanism through which the MCH1-R influences these behaviors remains unknown. MCH1-Rs are highly expressed in the nucleus accumbens shell (NAcSh) where they are co-expressed with dopamine (DA) receptors. MCH has been shown to potentiate responses to dopamine and to increase phosphorylation of DARPP-32, an intracellular marker of DA receptor activation, in the NAcSh.

methodsIn the present study, we investigated the role of the MCH1-R in alcohol reward using the conditioned place preference (CPP) paradigm. We then used immunohistochemistry (IHC) to assess activation of downstream signaling after administration of a rewarding dose of alcohol.

resultsWe found that alcohol-induced CPP was markedly decreased in mice with a genetic deletion of the MCH1-R as well as after pharmacological treatment with an MCH1-R antagonist, GW803430. In contrast, an isocaloric dose of dextrose did not produce CPP. The increase in DARPP-32 phosphorylation seen in wildtype (WT) mice after acute alcohol administration in the NAcSh was markedly reduced in MCH1-R knock-out (KO) mice.

conclusionOur results suggest that MCH1-Rs regulate the rewarding properties of alcohol through interactions with signaling cascades downstream of DA receptors in the NAcSh.

Indexed as

RewardAnimalsConditioning, PsychologicalDopamineDopamine and cAMP-Regulated Phosphoprotein 32EatingEthanolMaleMiceMice, Inbred C57BLMice, KnockoutNucleus AccumbensPhosphorylationReceptors, SomatostatinSelf AdministrationDopamineDopamine and cAMP-Regulated Phosphoprotein 32EthanolMchr1 protein, mousePpp1r1b protein, mouseReceptors, SomatostatinAlcoholConditioned place preference (CPP)Knock-out miceMCH1-Rp-DARPP-32Reward

Identifiers

PMID27044354
OpenAlexW2341137885

What OpenQuestion holds

Textmetadata
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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.