Evidence map›Paper›PMID 23148316›Full record

ArticleThe Journal of physiology2013

Dampened dopamine-mediated neuromodulation in prefrontal cortex of fragile X mice.

Kush Paul, Deepa V Venkitaramani, Charles L Cox

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Of Men and Mice: Modeling the Fragile X Syndrome.Frontiers in molecular neuroscience · 2018
    Article
  11. Article
  12. Article
  13. Review
  14. Differential effects of dopamine-directed treatments on cognition.Neuropsychiatric disease and treatment · 2015
    Review
  15. Review
  16. 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

3 authors at 2 institutions in 1 country.

Kush PaulDepartment of Molecular and Integrative Physiology, University of Illinois, Urbana, IL 61801, USA. kushpaul@illinois.edu
Deepa V Venkitaramani
Charles L Cox
University of Illinois Urbana-Champaign · USUrbana University · US

Funding

Restoring FMRP Phenotypes Frpm Temporal Regional and Splice- Isoforms VarationsP30HD002274 · NICHD · UNIVERSITY OF WASHINGTON · PI GURALNICK, MICHAEL J · 1985 to 2013
$33.6M
Modulation of Subcortical Visual Information ProcessingR01EY014024 · NEI · UNIVERSITY OF ILLINOIS URBANA-CHAMPAIGN · PI COX, CHARLES LEROY · 2003 to 2012
$2.6M
Synaptic Phenotype, Development, and Plasticity in the Fragile X MouseR01MH085324 · NIMH · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI COX, CHARLES LEROY · 2010 to 2015
$2.1M
Modulation of Subcortical Visual Information ProcessingR56EY014024 · NEI · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI COX, CHARLES LEROY · 2009 to 2009
$384k
NEI NIH HHS EY014024NEI NIH HHS R01 EY014024NEI NIH HHS R56 EY014024NICHD NIH HHS HD002274NICHD NIH HHS P30 HD002274NIMH NIH HHS MH085324NIMH NIH HHS R01 MH085324
6 · The paper itself

Abstract

Fragile X syndrome (FXS) is the most common form of inheritable mental retardation caused by transcriptional silencing of the Fmr1 gene resulting in the absence of fragile X mental retardation protein (FMRP). The role of this protein in neurons is complex and its absence gives rise to diverse alterations in neuronal function leading to neurological disorders including mental retardation, hyperactivity, cognitive impairment, obsessive-compulsive behaviour, seizure activity and autism. FMRP regulates mRNA translation at dendritic spines where synapses are formed, and thus the lack of FMRP can lead to disruptions in synaptic transmission and plasticity. Many of these neurological deficits in FXS probably involve the prefrontal cortex, and in this study, we have focused on modulatory actions of dopamine in the medial prefrontal cortex. Our data indicate that dopamine produces a long-lasting enhancement of evoked inhibitory postsynaptic currents (IPSCs) mediated by D1-type receptors seen in wild-type mice; however, such enhancement is absent in the Fmr1 knock-out (Fmr1 KO) mice. The facilitation of IPSCs produced by direct cAMP stimulation was unaffected in Fmr1 KO, but D1 receptor levels were reduced in these animals. Our results show significant disruption of dopaminergic modulation of synaptic transmission in the Fmr1 KO mice and this alteration in inhibitory activity may provide insight into potential targets for the rescue of deficits associated with FXS.

Indexed as

AnimalsDopamineFemaleFragile X Messenger Ribonucleoprotein 1Fragile X SyndromeInhibitory Postsynaptic PotentialsMaleMiceMice, KnockoutPrefrontal CortexPyramidal CellsReceptors, DopamineSynaptic TransmissionDopamineFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Receptors, Dopamine

Identifiers

PMID23148316
PMCPMC3591719
OpenAlexW1523697278

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.