Evidence map›Paper›PMID 29847232›Full record

ArticleJournal of neurophysiology2018

Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells.

Michael D Flood, Johnnie M Moore-Dotson, Erika D Eggers

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neurophysiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.9field-weighted citation impact, top 26% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

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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 1 institution in 1 country.

Michael D FloodDepartments of Physiology and Biomedical Engineering, University of Arizona , Tucson, Arizona.ORCID 0000-0001-8516-9582
Johnnie M Moore-DotsonDepartments of Physiology and Biomedical Engineering, University of Arizona , Tucson, Arizona.
Erika D EggersDepartments of Physiology and Biomedical Engineering, University of Arizona , Tucson, Arizona.ORCID 0000-0003-1465-7284
University of Arizona · US

Funding

PHYSIOLOGYT32HL007249 · NHLBI · UNIVERSITY OF ARIZONA · PI Brett A Colson, JOHN P KONHILAS · 1985 to 2026
$12.5M
Retinal Neuronal Signaling in Early DiabetesR01EY026027 · NEI · UNIVERSITY OF ARIZONA · PI EGGERS, ERIKA D. · 2016 to 2024
$2.9M
NEI NIH HHS R01 EY026027NHLBI NIH HHS T32 HL007249
6 · The paper itself

Abstract

Dopamine modulation of retinal signaling has been shown to be an important part of retinal adaptation to increased background light levels, but the role of dopamine modulation of retinal inhibition is not clear. We previously showed that light adaptation causes a large reduction in inhibition to rod bipolar cells, potentially to match the decrease in excitation after rod saturation. In this study, we determined how dopamine D1 receptors in the inner retina contribute to this modulation. We found that D1 receptor activation significantly decreased the magnitude of inhibitory light responses from rod bipolar cells, whereas D1 receptor blockade during light adaptation partially prevented this decline. To determine what mechanisms were involved in the modulation of inhibitory light responses, we measured the effect of D1 receptor activation on spontaneous currents and currents evoked from electrically stimulating amacrine cell inputs to rod bipolar cells. D1 receptor activation decreased the frequency of spontaneous inhibition with no change in event amplitudes, suggesting a presynaptic change in amacrine cell activity in agreement with previous reports that rod bipolar cells lack D1 receptors. Additionally, we found that D1 receptor activation reduced the amplitude of electrically evoked responses, showing that D1 receptors can modulate amacrine cells directly. Our results suggest that D1 receptor activation can replicate a large portion but not all of the effects of light adaptation, likely by modulating release from amacrine cells onto rod bipolar cells. NEW & NOTEWORTHY We demonstrated a new aspect of dopaminergic signaling that is involved in mediating light adaptation of retinal inhibition. This D1 receptor-dependent mechanism likely acts through receptors located directly on amacrine cells, in addition to its potential role in modulating the strength of serial inhibition between amacrine cells. Our results also suggest that another D2/D4 receptor-dependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

Indexed as

Adaptation, OcularNeural InhibitionAmacrine CellsAnimalsMaleMembrane PotentialsMice, Inbred C57BLModels, NeurologicalPhotic StimulationReceptors, Dopamine D1Retinal Bipolar CellsRetinal Rod Photoreceptor CellsReceptors, Dopamine D1adaptationamacrine celldopaminelight inhibitionrod bipolar cell

Identifiers

PMID29847232
PMCPMC6139461
OpenAlexW2805044115

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.