April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Evidence of Decreased Dopamine Receptor-Mediated Control of Gap Junction Coupling in the Inner Nuclear Layer of the Diabetic Ins2Akita Mouse Retina
Author Affiliations & Notes
  • Rene C Renteria
    Department of Physiology, The University of Texas Health Science Center at San Antonio, San Antonio, TX
  • Nikolay Akimov
    Department of Physiology, The University of Texas Health Science Center at San Antonio, San Antonio, TX
  • Zhijing Zhang
    Department of Ophthalmology & Visual Science, University of Texas Health Science Center, Houston, Houston, TX
  • Christophe Ribelayga
    Department of Ophthalmology & Visual Science, University of Texas Health Science Center, Houston, Houston, TX
  • Monika Pyarali
    Department of Physiology, The University of Texas Health Science Center at San Antonio, San Antonio, TX
  • Lourdes A Fortepiani
    Rosenberg School of Optometry, University of the Incarnate Word, San Antonio, TX
  • Footnotes
    Commercial Relationships Rene Renteria, None; Nikolay Akimov, None; Zhijing Zhang, None; Christophe Ribelayga, None; Monika Pyarali, None; Lourdes Fortepiani, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1067. doi:
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      Rene C Renteria, Nikolay Akimov, Zhijing Zhang, Christophe Ribelayga, Monika Pyarali, Lourdes A Fortepiani; Evidence of Decreased Dopamine Receptor-Mediated Control of Gap Junction Coupling in the Inner Nuclear Layer of the Diabetic Ins2Akita Mouse Retina. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1067.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: Dopamine is a light-adaptive factor under circadian control that plays an important role in daytime vision and in the transition from nighttime vision. Dopamine controls the gain of retinal signal transmission partly by controlling gap junction coupling of several different retinal neuron networks. Our preliminary evidence suggests that dopamine production is impaired in the retina of the hyperglycemic Ins2Akita mouse, a model of diabetes. Here we begin to test the hypothesis that gap junction coupling is altered in diabetic retina due to this tonic reduction in retinal dopamine.

Methods: We assayed coupling using a “cut-loading” technique, in which whole-mounted retinas are cut with a razor dipped in the gap junction-permeable tracer Neurobiotin (NB), and quantified NB-labeled cells in the inner nuclear layer (INL) using fluorescence microscopy. The retinas were from mice dark-adapted for a set time period during a similar time of day and were maintained under dim red illumination during loading procedures. The extent of coupling in control (C57Bl6) retinas was tested in the presence of the dopamine D2-like receptor (D2R) agonist quinpirole (Qnp), the D2R antagonist sulpiride (Sulp), or the gap junction antagonist beta-glycyrrhizic acid (BGA).

Results: Consistent with previous studies, D2R activation and BGA each significantly reduced gap junction coupling in normal retinas, as indicated by fewer NB-labeled cells detected in the INL compared to controls (Ctrl) (mean ± stdev, NB cells per square 100 µm: Qnp, 4.2 ± 0.5; BGA, 2.7 ± 0.3; Ctrl, 7.6 ± 0.4). In contrast, D2R antagonism significantly increased tracer coupling in normal retinas (Sulp, 12.8 ± 0.6). In retinas from diabetic Ins2Akita mice (Diab), we found greater numbers of NB-labeled cells in the INL, indicating increased tracer coupling, compared to non-diabetic littermates (littermate Ctrl, 8.3 ± 0.9; Diab, 10.5 ± 1.0; p < 0.001).

Conclusions: We propose that this increase in gap junction coupling between retinal neurons is a result of a decrease in dopamine levels in the diabetic retina. Decreased dopamine levels and an altered coupling state of retinal neurons may be hallmarks of the retina during diabetes.

Keywords: 499 diabetic retinopathy • 562 inner retina dysfunction: biochemistry and cell biology • 532 gap junctions/coupling  
×
×

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.

×