May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Dopamine Released During Subjective Twilight Suppresses the Saturating Rod B–wave Amplitude of the Rat Electroretinogram
Author Affiliations & Notes
  • J.D. Akula
    Department of Psychology, Northeastern University, Boston, MA
  • M.E. Rice
    Department of Physiology and Neuroscience, New York University School of Medicine, New York, NY
  • F. Naarendorp
    Department of Psychology, Northeastern University, Boston, MA
  • Footnotes
    Commercial Relationships  J.D. Akula, None; M.E. Rice, None; F. Naarendorp, None.
  • Footnotes
    Support  NIH Grant EY14057
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 5695. doi:
  • Views
  • Share
  • Tools
    • Alerts
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      J.D. Akula, M.E. Rice, F. Naarendorp; Dopamine Released During Subjective Twilight Suppresses the Saturating Rod B–wave Amplitude of the Rat Electroretinogram . Invest. Ophthalmol. Vis. Sci. 2005;46(13):5695.

      Download citation file:

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

  • Supplements

Abstract: : Purpose: To assess the effects of endogenous dopamine (DA) on the outer retinal division of the primary rod pathway. Background: Rod signals elicited with dim stimuli are transmitted through the retina in the pathway that initiates at the rod–rod bipolar cell (RBC) synapse. Because of significant rod–signal convergence, the RBC response saturates to moderate (twilight) stimuli. Endogenous DA released by a subset of amacrine cells in twilight might further reduce the signal flow through the rod bipolar pathway.+ Assuming that the rod b–wave of the electroretinogram (ERG) is generated by RBCs, we examine whether fluctuations of the saturating b–wave amplitude correlate with DA release. Methods: Using standard recording techniques, ERGs were obtained from anesthetized dark–adapted adult rats, at preset circadian times (CT). ERGs were also recorded in the presence of DA agonists or antagonists, and after treatment with 6–hydroxydopamine (6–OHDA). Eyes were enucleated at preset CTs; DA and DOPAC concentrations were then measured by HPLC. Circadian times were determined from actograms of wheel running by rats kept in continuous darkness. Results: (1) V log I curves for rod b–waves obtained during subjective night (SN) were well described by the Michaelis–Menten equation (n=5). Flashes producing 10–20 photoisomerizations (R*) saturate the rod b–wave. During subjective twilight (ST), responses elicited with flashes producing ≤ 10 R* were indistinguishable from those obtained during SN. However, responses elicited with ‘mesopic’ flashes (producing 20–200 R*) were reduced by about 15–25%. (2) Quinpirole [∼15 µM], a D2 agonist, applied during SN reduced the response amplitude to mesopic flashes by 20%. L–745,870 [∼25 µM], a D4 antagonist, applied during ST, reduced suppression of the saturating b–wave. (3) V log I curves obtained from eyes treated with 6–OHDA (n=3) during ST and SN resembled those obtained from controls during SN. (4) DA concentration during ST was twice as high as during SN (n=10). The DA/DOPAC ratio was also larger during ST. Conclusions: The signal flow through the primary rod pathway is suppressed by endogenous DA in twilight. Whether DA facilitates rerouting of the rod signal to the second rod pathway is yet to be determined. +Witkovsky P. Dopamine and retinal function. Doc Ophthalmol. 2004; 108:17–40.

Keywords: electroretinography: non-clinical • dopamine • circadian rhythms 

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.