Evidence map›Paper›PMID 25716863›Full record

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

Absence of plateau potentials in dLGN cells leads to a breakdown in retinogeniculate refinement.

Emily K Dilger, Thomas E Krahe, Duncan R Morhardt, Tania A Seabrook, Hee-Sup Shin, William Guido

Abstract 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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
–field-weighted citation impact
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

23 citing papers in PubMed.

  1. Article
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  10. Article
  11. Review
  12. Article
  13. Article
  14. Thalamocortical function in developing sensory circuits.Current opinion in neurobiology · 2018
    Review
  15. Review
  16. Article
  17. Activity-dependent development of visual receptive fields.Current opinion in neurobiology · 2017
    Review
  18. Article
  19. Review
  20. Review
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

6 authors.

Emily K DilgerDepartment of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298.
Thomas E KraheDepartment of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298.
Duncan R MorhardtDepartment of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298.
Tania A SeabrookDepartment of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298, Department of Anatomical Sciences and Neurobiology, University of Louisville, School of Medicine, Health Sciences Center, Louisville, Kentucky 40292.ORCID http://orcid.org/0000-0001-6392-1948
Hee-Sup ShinBrain Science Institute, Korea Institute of Science and Technology, Seoul 136-791, Republic of Korea, and.
William GuidoDepartment of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, Virginia 23298, Department of Anatomical Sciences and Neurobiology, University of Louisville, School of Medicine, Health Sciences Center, Louisville, Kentucky 40292 william.guido@louisville.edu.

Funding

FUNCTIONAL STATE OF DEVELOPING RETINOGENICULATE SYNAPSER01EY012716 · NEI · VIRGINIA COMMONWEALTH UNIVERSITY · PI GUIDO, WILLIAM · 2001 to 2021
$6.9M
NEI NIH HHS EY12716NEI NIH HHS R01 EY012716
6 · The paper itself

Abstract

The link between neural activity and the refinement of projections from retina to the dorsal lateral geniculate nucleus (dLGN) of thalamus is based largely on studies that disrupt presynaptic retinogeniculate activity. Postsynaptic mechanisms responsible for implementing the activity-dependent remodeling in dLGN remain unknown. We tested whether L-type Ca(2+) channel activity in the form of synaptically evoked plateau potentials in dLGN cells is needed for remodeling by using a mutant mouse that lacks the ancillary β3 subunit and, as a consequence, has highly reduced L-type channel expression and attenuated L-type Ca(2+) currents. In the dLGNs of β3-null mice, glutamatergic postsynaptic activity evoked by optic tract stimulation was normal, but plateau potentials were rarely observed. The few plateaus that were evoked required high rates of retinal stimulation, but were still greatly attenuated compared with those recorded in age-matched wild-type mice. While β3-null mice exhibit normal stage II and III retinal waves, their retinogeniculate projections fail to segregate properly and dLGN cells show a high degree of retinal convergence even at late postnatal ages. These structural and functional defects were also accompanied by a reduction in CREB phosphorylation, a signaling event that has been shown to be essential for retinogeniculate axon segregation. Thus, postsynaptic L-type Ca(2+) activity plays an important role in mediating the refinement of the retinogeniculate pathway.

Indexed as

Excitatory Postsynaptic PotentialsAnimalsCalcium Channels, L-TypeCyclic AMP Response Element-Binding ProteinFemaleGeniculate BodiesMaleMiceMice, Inbred C57BLPhosphorylationProtein SubunitsRetinal Ganglion CellsVisual PathwaysCalcium Channels, L-TypeCyclic AMP Response Element-Binding ProteinProtein Subunitsactivity-dependent refinementlateral geniculate nucleusl-type Ca2+ channelretinaretinogeniculateβ3-null mice

Identifiers

PMID25716863
PMCPMC4339365

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.