Evidence map›Paper›PMID 28083675›Full record

ArticlePsychopharmacology2017

Assessment of a glycine uptake inhibitor in animal models of effort-related choice behavior: implications for motivational dysfunctions.

Samantha E Yohn, Daniela Alberati, Merce Correa, John D Salamone

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Article in Psychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

5 citing papers in PubMed, 15 citations in OpenAlex.

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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

4 authors at 3 institutions in 3 countries.

Samantha E YohnDivision of Behavioral Neuroscience, Department of Psychological Sciences, University of Connecticut, Storrs, CT, 06269-1020, USA.
Daniela AlberatiF. Hoffmann-La Roche, Neuroscience, Ophthalmology and Rare Diseases, Pharma Research and Early Development, Grenzacherstrasse 124, CH4070, Basel, Switzerland.
Merce CorreaDivision of Behavioral Neuroscience, Department of Psychological Sciences, University of Connecticut, Storrs, CT, 06269-1020, USA.
John D SalamoneDivision of Behavioral Neuroscience, Department of Psychological Sciences, University of Connecticut, Storrs, CT, 06269-1020, USA. john.salamone@uconn.edu.
University of Connecticut · USRoche (Switzerland) · CHUniversitat Jaume I · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleMotivated behavior can be characterized by a substantial exertion of effort, and organisms often make effort-related decisions based upon analyses of work-related response costs and reinforcement preference. Moreover, alterations in effort-based choice can be seen in people with major depression and schizophrenia. Effort-related decision making is studied using tasks offering choices between high effort options leading to highly valued reinforces vs low effort/low reward options. Interference with dopamine (DA) transmission by administration of the DA D2 family antagonist haloperidol biases behavior towards the lower effort option that can be obtained with minimal work, and previous research has shown that DA interacts with other transmitters, including adenosine and GABA, to regulate effort-based choice.

objectivesThe present studies focused upon the ability of the glycine transport inhibitor bitopertin to attenuate haloperidol-induced shifts in effort-related choice behavior.

methodsEffort-based choice in rats was assessed using the concurrent fixed ratio (FR) 5/chow feeding choice task and the T-maze barrier choice procedure.

resultsHaloperidol shifted effort-based choice, biasing animals towards the low effort option in each task. Co-administration of bitopertin (1.0-10.0 mg/kg) significantly attenuated haloperidol-induced shifts in choice behavior, but the same doses of bitopertin had no effect when administered alone.

conclusionsThese results indicated that elevation of extracellular glycine via inhibition of glycine uptake was able to reverse the effects of D2 antagonism. Increases in extracellular glycine, possibly through actions on the glycine allosteric site on the NMDA receptor, may be a useful strategy for treating motivational dysfunctions in humans.

Indexed as

Models, AnimalAnimalsChoice BehaviorDopamineDopamine AntagonistsDose-Response Relationship, DrugGlycineHaloperidolMajor Depressive DisorderMaleMotivationPiperazinesRatsRats, Sprague-DawleyRewardSulfones(4-(3-fluoro-5-trifluoromethylpyridin-2-yl)piperazin-1-yl)(5-methanesulfonyl-2-(2,2,2-trifluoro-1-methylethoxy)phenyl)methanoneDopamineDopamine AntagonistsGlycineHaloperidolPiperazinesSulfonesAnergiaDopamineFatigueGlycine uptakeMotivationNMDA

Identifiers

PMID28083675
OpenAlexW2575990521

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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.