Evidence map›Paper›PMID 25008417›Full record

ArticleJournal of neurophysiology2014

Intrinsic bursting of AII amacrine cells underlies oscillations in the rd1 mouse retina.

Hannah Choi, Lei Zhang, Mark S Cembrowski, Carl F Sabottke, Alexander L Markowitz, Daniel A Butts, William L Kath, Joshua H Singer, Hermann Riecke

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

64 citing papers in PubMed, 95 citations in OpenAlex.

  1. Dopamine suppresses pathological retinal oscillations and enhances the signal-to-noise ratio.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  15. A retinal origin of nystagmus-a perspective.Frontiers in ophthalmology · 2023
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4 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 1 country.

Hannah ChoiDepartment of Engineering Sciences and Applied Mathematics, Northwestern University, Evanston, Illinois;
Lei ZhangDepartment of Biology, University of Maryland, College Park, Maryland; and.
Mark S CembrowskiHoward Hughes Medical Institute, Janelia Farm Research Campus, Ashburn, Virginia.
Carl F SabottkeDepartment of Biology, University of Maryland, College Park, Maryland; and.
Alexander L MarkowitzDepartment of Biology, University of Maryland, College Park, Maryland; and.
Daniel A ButtsDepartment of Biology, University of Maryland, College Park, Maryland; and.
William L KathDepartment of Engineering Sciences and Applied Mathematics, Northwestern University, Evanston, Illinois;
Joshua H SingerDepartment of Biology, University of Maryland, College Park, Maryland; and.
Hermann RieckeDepartment of Engineering Sciences and Applied Mathematics, Northwestern University, Evanston, Illinois; h-riecke@northwestern.edu.
University of Maryland, College Park · USNorthwestern University · USJanelia Research Campus · US

Funding

Synaptic Transmission in The Rod Pathway of the Mammalian RetinaR01EY017836 · NEI · UNIV OF MARYLAND, COLLEGE PARK · PI Jonathan B Demb, Anastas Popratiloff · 2007 to 2026
$7.2M
CRCNS: Biophysical properties of parallel neural circuits serving night visionR01EY021372 · NEI · UNIV OF MARYLAND, COLLEGE PARK · PI DEMB, JONATHAN B, SINGER, JOSHUA H · 2010 to 2016
$2.1M
NEI NIH HHS EY-017836NEI NIH HHS EY-021372
6 · The paper itself

Abstract

In many forms of retinal degeneration, photoreceptors die but inner retinal circuits remain intact. In the rd1 mouse, an established model for blinding retinal diseases, spontaneous activity in the coupled network of AII amacrine and ON cone bipolar cells leads to rhythmic bursting of ganglion cells. Since such activity could impair retinal and/or cortical responses to restored photoreceptor function, understanding its nature is important for developing treatments of retinal pathologies. Here we analyzed a compartmental model of the wild-type mouse AII amacrine cell to predict that the cell's intrinsic membrane properties, specifically, interacting fast Na and slow, M-type K conductances, would allow its membrane potential to oscillate when light-evoked excitatory synaptic inputs were withdrawn following photoreceptor degeneration. We tested and confirmed this hypothesis experimentally by recording from AIIs in a slice preparation of rd1 retina. Additionally, recordings from ganglion cells in a whole mount preparation of rd1 retina demonstrated that activity in AIIs was propagated unchanged to elicit bursts of action potentials in ganglion cells. We conclude that oscillations are not an emergent property of a degenerated retinal network. Rather, they arise largely from the intrinsic properties of a single retinal interneuron, the AII amacrine cell.

Indexed as

Action PotentialsAmacrine CellsAnimalsCyclic Nucleotide Phosphodiesterases, Type 6Excitatory Postsynaptic PotentialsMembrane PotentialsMiceModels, NeurologicalPotassiumRetinal Cone Photoreceptor CellsRetinal DegenerationRetinal Ganglion CellsSodiumCyclic Nucleotide Phosphodiesterases, Type 6Pde6b protein, mousePotassiumSodiumAII amacrine cellburstingoscillationretinal degeneration

Identifiers

PMID25008417
PMCPMC4137253
OpenAlexW2141112752

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.