Evidence map›Paper›PMID 27003189›Full record

ArticleTranslational psychiatry2016

Functional magnetic resonance imaging in awake transgenic fragile X rats: evidence of dysregulation in reward processing in the mesolimbic/habenular neural circuit.

W M Kenkel, J R Yee, K Moore, D Madularu, P Kulkarni, K Gamber, M Nedelman, C F Ferris

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 6% 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

22 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.

  1. Where do we stand on fMRI in awake mice?Cerebral cortex (New York, N.Y. : 1991) · 2024
    Pooled it
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  20. Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018
    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

8 authors at 3 institutions in 2 countries.

W M KenkelThe Kinsey Institute, Indiana University, Bloomington, IN, USA.
J R YeeThe Kinsey Institute, Indiana University, Bloomington, IN, USA.
K MooreDepartment of Psychology, Center for Translational NeuroImaging, Northeastern University, Boston, MA, USA.
D MadularuBrain Imaging Centre, Douglas Mental Health University Institute, McGill University, Montreal, QC, Canada.
P KulkarniDepartment of Psychology, Center for Translational NeuroImaging, Northeastern University, Boston, MA, USA.
K GamberSAGE Labs, St Louis, MO, USA.
M NedelmanEkam Imaging, Boston, MA, USA.
C F FerrisDepartment of Psychology, Center for Translational NeuroImaging, Northeastern University, Boston, MA, USA.
Northeastern University · USIndiana University Bloomington · USDouglas Mental Health University Institute · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anxiety and social deficits, often involving communication impairment, are fundamental clinical features of fragile X syndrome. There is growing evidence that dysregulation in reward processing is a contributing factor to the social deficits observed in many psychiatric disorders. Hence, we hypothesized that transgenic fragile X mental retardation 1 gene (fmr1) KO (FX) rats would display alterations in reward processing. To this end, awake control and FX rats were imaged for changes in blood oxygen level dependent (BOLD) signal intensity in response to the odor of almond, a stimulus to elicit the innate reward response. Subjects were 'odor naive' to this evolutionarily conserved stimulus. The resulting changes in brain activity were registered to a three-dimensional segmented, annotated rat atlas delineating 171 brain regions. Both wild-type (WT) and FX rats showed robust brain activation to a rewarding almond odor, though FX rats showed an altered temporal pattern and tended to have a higher number of voxels with negative BOLD signal change from baseline. This pattern of greater negative BOLD was especially apparent in the Papez circuit, critical to emotional processing and the mesolimbic/habenular reward circuit. WT rats showed greater positive BOLD response in the supramammillary area, whereas FX rats showed greater positive BOLD response in the dorsal lateral striatum, and greater negative BOLD response in the retrosplenial cortices, the core of the accumbens and the lateral preoptic area. When tested in a freely behaving odor-investigation paradigm, FX rats failed to show the preference for almond odor which typifies WT rats. However, FX rats showed investigation profiles similar to WT when presented with social odors. These data speak to an altered processing of this highly salient novel odor in the FX phenotype and lend further support to the notion that altered reward systems in the brain may contribute to fragile X syndrome symptomology.

Indexed as

RewardAnimalsAnimals, Genetically ModifiedBrainFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeFunctional NeuroimagingHabenulaHypothalamusMagnetic Resonance ImagingMaleNeural PathwaysNucleus AccumbensRatsRats, Sprague-DawleySubstantia NigraFragile X Messenger Ribonucleoprotein 1

Identifiers

PMID27003189
PMCPMC4872441
OpenAlexW2306100596

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LicenceCC BY
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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.