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

Research output: Contribution to journalArticle

2 Citations (Scopus)

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 receptordependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

Original languageEnglish (US)
Pages (from-to)867-879
Number of pages13
JournalJournal of Neurophysiology
Volume120
Issue number2
DOIs
StatePublished - Aug 15 2018

Fingerprint

Amacrine Cells
Dopamine D1 Receptors
Ocular Adaptation
Light
Dopamine
Retina

Keywords

  • Adaptation
  • Amacrine cell
  • Dopamine
  • Light inhibition
  • Rod bipolar cell

ASJC Scopus subject areas

  • Neuroscience(all)
  • Physiology

Cite this

Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells. / Flood, Michael D.; Moore-Dotson, Johnnie M.; Eggers, Erika D.

In: Journal of Neurophysiology, Vol. 120, No. 2, 15.08.2018, p. 867-879.

Research output: Contribution to journalArticle

@article{995f7b61a2f64163b513975486838c1a,
title = "Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells",
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 receptordependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.",
keywords = "Adaptation, Amacrine cell, Dopamine, Light inhibition, Rod bipolar cell",
author = "Flood, {Michael D.} and Moore-Dotson, {Johnnie M.} and Eggers, {Erika D}",
year = "2018",
month = "8",
day = "15",
doi = "10.1152/jn.00855.2017",
language = "English (US)",
volume = "120",
pages = "867--879",
journal = "Journal of Neurophysiology",
issn = "0022-3077",
publisher = "American Physiological Society",
number = "2",

}

TY - JOUR

T1 - Dopamine D1 receptor activation contributes to light-adapted changes in retinal inhibition to rod bipolar cells

AU - Flood, Michael D.

AU - Moore-Dotson, Johnnie M.

AU - Eggers, Erika D

PY - 2018/8/15

Y1 - 2018/8/15

N2 - 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 receptordependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

AB - 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 receptordependent or dopamine-independent mechanism must also be involved in light adaptation of inhibition to rod bipolar cells.

KW - Adaptation

KW - Amacrine cell

KW - Dopamine

KW - Light inhibition

KW - Rod bipolar cell

UR - http://www.scopus.com/inward/record.url?scp=85052154033&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85052154033&partnerID=8YFLogxK

U2 - 10.1152/jn.00855.2017

DO - 10.1152/jn.00855.2017

M3 - Article

C2 - 29847232

AN - SCOPUS:85052154033

VL - 120

SP - 867

EP - 879

JO - Journal of Neurophysiology

JF - Journal of Neurophysiology

SN - 0022-3077

IS - 2

ER -