July 2019
Volume 60, Issue 9
Open Access
ARVO Annual Meeting Abstract  |   July 2019
Endogenous Adenosine-Mediated Suppression of ipRGC Photoresponses during Dark Adaptation
Author Affiliations & Notes
  • Phillip Thomas Yuhas
    Optometry, The Ohio State University College of Optometry, Columbus, Ohio, United States
  • Puneet Sodhi
    BioMotiv, Shaker Heights, Ohio, United States
  • Andrew Hartwick
    Optometry, The Ohio State University College of Optometry, Columbus, Ohio, United States
  • Footnotes
    Commercial Relationships   Phillip Yuhas, None; Puneet Sodhi, None; Andrew Hartwick, None
  • Footnotes
    Support  Grant 8KL2TR000112-05 from National Center for Advancing Translational Sciences, Ohio State Alumni Grant for Graduate Research and Scholarship
Investigative Ophthalmology & Visual Science July 2019, Vol.60, 5260. doi:
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      Phillip Thomas Yuhas, Puneet Sodhi, Andrew Hartwick; Endogenous Adenosine-Mediated Suppression of ipRGC Photoresponses during Dark Adaptation. Invest. Ophthalmol. Vis. Sci. 2019;60(9):5260.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose : We have previously demonstrated that pharmacological activation of adenosine A1 receptors suppresses light-evoked ipRGC firing. As environmental lighting conditions are known to modulate retinal adenosine levels, here we examined whether prolonged dark adaptation affects rat ipRGC photoresponses through an adenosine-mediated mechanism.

Methods : Eyes from postnatal (8-13 day old) and adult (>2 months) Long-Evans rats were dissected and retinas were placed RGC-side down on 60-electrode arrays (Multichannel Systems, Germany). Retinas were dark adapted for in Hibernate-A medium for 2.5 h before first light exposure, with either adenosine transport inhibitor NMBPR (20 μM) alone or with NMBPR and adenosine A1 antagonist DPCPX (20 μM). Retinas were then superfused with heated, oxygenated Ames medium for 20 min and a series of 5 successive 20 s bright (7x1015 phots/s/cm2), blue (470 nm) light pulses were presented, separated by 5 min darkness.

Results : In the presence of NMBPR alone, dark adaptation led to a suppression of mean peak firing frequency and total spikes fired in light-evoked ipRGCs. There was a significant increase (p<0.001) in the mean number of spikes fired in response to the fifth pulse (184.0 ± 14.4), as compared to the first pulse (71.8 ± 19.2), in the neonatal ipRGCs (n=15). A similar significant (p=0.04) increase in spikes fired to the last pulse (330.4 ± 144.1) from the first (55.6 ± 43.1) pulse in the adult ipRGCs (n=5). This suppression of ipRGC spiking responses to the initial stimuli after prolonged dark adaptation did not occur in retinas treated with DPCPX, as no significant difference (p>0.05) was observed from initial (295.9 ± 19.5; 195.7 ± 90.1) spike counts to those evoked by the final pulse (306 ± 15.5; 242.3 ± 80.3) of light in neonatal (n=64) and adult (n=6) ipRGCs, respectively.

Conclusions : These results indicate endogenous adenosine accumulation following dark adaptation induces global suppression of ipRGC light responses through activation of the A1 receptor. Thus, the gain of ipRGC light responses is not a static characteristic, but instead is regulated by light-and circadian-driven changes in extracellular retinal levels of adenosine and other cAMP-related neuromodulators.

This abstract was presented at the 2019 ARVO Annual Meeting, held in Vancouver, Canada, April 28 - May 2, 2019.


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