Evidence map›Paper›PMID 25653361›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015

Impaired presynaptic long-term potentiation in the anterior cingulate cortex of Fmr1 knock-out mice.

Kohei Koga, Ming-Gang Liu, Shuang Qiu, Qian Song, Gerile O'Den, Tao Chen, Min Zhuo

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

40 citing papers in PubMed, 63 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. An Out-of-Place Etiology: Recognizing FMR1 Premutation in the Memory Clinic.Annals of clinical and translational neurology · 2026
    Article
  5. Review
  6. Article
  7. Cortical Tagged Synaptic Long-Term Depression in the Anterior Cingulate Cortex of Adult Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  8. Cage effects on synaptic plasticity and its modulation in a mouse model of fragile X syndrome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  9. Cortical nitric oxide required for presynaptic long-term potentiation in the insular cortex.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. TRPA1 as a OScientific reports · 2023
    Article
  15. Mouse models of fragile X-related disorders.Disease models & mechanisms · 2023
    Review
  16. Article
  17. Review
  18. Hyperexcitability and Homeostasis in Fragile X Syndrome.Frontiers in molecular neuroscience · 2021
    Article
  19. Review
  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

7 authors at 3 institutions in 2 countries.

Kohei KogaDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, Toronto, Ontario, M5S 1A8, Canada, Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, Shanxi 710049, China.
Ming-Gang LiuDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, Toronto, Ontario, M5S 1A8, Canada, Department of Anatomy and Histology and Embryology, Institute of Medical Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China, and.
Shuang QiuDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, Toronto, Ontario, M5S 1A8, Canada, Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, Shanxi 710049, China.
Qian SongDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, Toronto, Ontario, M5S 1A8, Canada, Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, Shanxi 710049, China.
Gerile O'DenCenter for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, Shanxi 710049, China.
Tao ChenDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, Toronto, Ontario, M5S 1A8, Canada, Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, Shanxi 710049, China, Department of Anatomy and KK Leung Brain Research Center, Fourth Military Medical University, Xi'an, Shanxi 710032, China.
Min ZhuoDepartment of Physiology, Faculty of Medicine, University of Toronto, Medical Science Building, Toronto, Ontario, M5S 1A8, Canada, Center for Neuron and Disease, Frontier Institutes of Science and Technology, Xi'an Jiaotong University, Xi'an, Shanxi 710049, China, min.zhuo@utoronto.ca.
Xi'an Jiaotong University · CNUniversity of Toronto · CAAir Force Medical University · CN

Funding

Canadian Institutes of Health Research MOP-124807
6 · The paper itself

Abstract

Fragile X syndrome is a common inherited form of mental impairment. Fragile X mental retardation protein (FMRP) plays important roles in the regulation of synaptic protein synthesis, and loss of FMRP leads to deficits in learning-related synaptic plasticity and behavioral disability. Previous studies mostly focus on postsynaptic long-term potentiation (LTP) in Fmr1 knock-out (KO) mice. Here, we investigate the role of FMRP in presynaptic LTP (pre-LTP) in the adult mouse anterior cingulate cortex (ACC). Low-frequency stimulation induced LTP in layer II/III pyramidal neurons under the voltage-clamp mode. Paired-pulse ratio, which is a parameter for presynaptic changes, was decreased after the low-frequency stimulation in Fmr1 wild-type (WT) mice. Cingulate pre-LTP was abolished in Fmr1 KO mice. We also used a 64-electrode array system for field EPSP recording and found that the combination of low-frequency stimulation paired with a GluK1-containing kainate receptor agonist induced NMDA receptor-independent and metabotropic glutamate receptor-dependent pre-LTP in the WT mice. This potentiation was blocked in Fmr1 KO mice. Biochemical experiments showed that Fmr1 KO mice displayed altered translocation of protein kinase A subunits in the ACC. Our results demonstrate that FMRP plays an important role in pre-LTP in the adult mouse ACC, and loss of this pre-LTP may explain some of the behavioral deficits in Fmr1 KO mice.

Indexed as

Long-Term PotentiationAnimalsCyclic AMP-Dependent Protein KinasesExcitatory Postsynaptic PotentialsFragile X Messenger Ribonucleoprotein 1Gyrus CinguliKainic Acid ReceptorsMaleMiceMice, KnockoutPyramidal CellsReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartateSynapsesCyclic AMP-Dependent Protein KinasesFmr1 protein, mouseFragile X Messenger Ribonucleoprotein 1Kainic Acid ReceptorsReceptors, Metabotropic GlutamateReceptors, N-Methyl-D-AspartatecortexFMRPfragile X diseaseLTPmicePKA

Identifiers

PMID25653361
PMCPMC6705363
OpenAlexW1964400547

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.