April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Feedback Control Of Rod Photoreceptor Synaptic Output By Hcn1 Channels Is Essential For A Regular Rod-Cone Interaction In The Mammalian Retina
Author Affiliations & Notes
  • Mathias W. Seeliger
    Division of Ocular Neurodegeneration, Ctr Ophthalmology Inst Ophthalmic Research, Tuebingen, Germany
  • Naoyuki Tanimoto
    Division of Ocular Neurodegeneration, Ctr Ophthalmology Inst Ophthalmic Research, Tuebingen, Germany
  • Arne Brombas
    Forschungszentrum Juelich, Institut fuer Strukturbiologie und Biophysik (ISB-1), Juelich, Germany
  • Reto Weiler
    Neurobiology, University of Oldenburg, Oldenburg, Germany
  • Peter Humphries
    Ocular Genetics Unit, Trinity College Dublin, Dublin, Ireland
  • Frank Mueller
    Forschungszentrum Juelich, Institut fuer Strukturbiologie und Biophysik (ISB-1), Juelich, Germany
  • Footnotes
    Commercial Relationships  Mathias W. Seeliger, None; Naoyuki Tanimoto, None; Arne Brombas, None; Reto Weiler, None; Peter Humphries, None; Frank Mueller, None
  • Footnotes
    Support  DFG grants Se837/5-2 & Se837/6-1 and European Union grant (EVI-Genoret LSHG-CT-2005-512036)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 6580. doi:
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      Mathias W. Seeliger, Naoyuki Tanimoto, Arne Brombas, Reto Weiler, Peter Humphries, Frank Mueller; Feedback Control Of Rod Photoreceptor Synaptic Output By Hcn1 Channels Is Essential For A Regular Rod-Cone Interaction In The Mammalian Retina. Invest. Ophthalmol. Vis. Sci. 2011;52(14):6580.

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

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Abstract

Purpose: : To show that under conditions where both rods and cones are active, the internal feedback provided by HCN1 channels in rod photoreceptors is essential to allow cone-mediated vision, and to identify key components of the underlying functional rod-cone interaction.

Methods: : The hypothesis that rod-cone interaction requires a transmission of the electrical signal via Cx36 gap junctions was assessed using wild-type and transgenic mice with specific functional characteristics (Hcn1-/-, prolonged photoresponses; Cx36-/-, no connexin36-mediated gap junctions; rho-/-, no rod function) and two types of double mutant mice (Hcn1-/-Cx36-/-; Hcn1-/-rho-/-). Mice were examined in vivo with Ganzfeld flicker electroretinography (ERG) and in vitro with patch-clamp studies in retinal whole-mount preparations.

Results: : We found that (a) normal rod photoreceptor output is intrinsically controlled by HCN1 channel feedback, (b) lack of HCN1 channel feedback leads to exaggerated, prolonged rod responses, (c) prolonged rod responses saturate the retinal network and block cone signal flow, and (d) genetical or pharmacological ablation of rod-cone connections restores cone signaling.

Conclusions: : In summary, exaggerated rod responses following bright light exposure in the absence of HCN1 channels saturate the retinal network, resulting in an almost complete suppression of cone signals. By specific genetic and pharmacological ablation of key signal processing components, we were able to restore regular cone signaling, thereby identifying the sites involved in functional rod-cone interaction.

Keywords: retinal connections, networks, circuitry • retina: distal (photoreceptors, horizontal cells, bipolar cells) • gap junctions/coupling 
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