December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Role of AII Amacrine Cell Coupling in Rod Vision: Studies Using a Connexin36 Knockout Mouse
Author Affiliations & Notes
  • B Volgyi
    Ophthalmology Physiology & Neuroscience NYU School of Medicine New York NY
  • M Deans
    Neurobiology Harvard Medical School Boston MA
  • D Paul
    Neurobiology Harvard Medical School Boston MA
  • SA Bloomfield
    Ophthalmology Physiology & Neuroscience NYU School of Medicine New York NY
  • Footnotes
    Commercial Relationships   B. Volgyi, None; M. Deans, None; D. Paul, None; S.A. Bloomfield, None. Grant Identification: Support: NIH Grants EY07360, GM37751, Fight for Sight and Ilfeld Macular Degeneration Res. Fund
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 1944. doi:
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      B Volgyi, M Deans, D Paul, SA Bloomfield; Role of AII Amacrine Cell Coupling in Rod Vision: Studies Using a Connexin36 Knockout Mouse . Invest. Ophthalmol. Vis. Sci. 2002;43(13):1944.

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

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Abstract: : Purpose: To study the role of AII amacrine cell gap junctions in the transmission and processing of rod signals. Methods: Experiments were performed on wild-type (WT) and connexin36 (Cx36) knockout (KO) mice, the latter which lack AII-AII and AII-cone bipolar cell gap junctions. Extracellular recordings were obtained from retinal ganglion cells under infrared illumination in an in vitro, superfused retina-eyecup preparation. Ganglion cell spiking in response to calibrated full-field light stimuli was quantified to produce intensity-response functions. Results: On-center ganglion cells in WT mice formed basically 2 populations based on differences in intensity-response functions. One group displayed very low thresholds (0.1-0.5 Rh*/rod/sec), whereas the second showed thresholds about 2.5 log units higher. The off-center ganglion cells in the WT mouse also showed low and high threshold groups that corresponded to the on-center cells, but there were also cells with more intermediate intensity-response functions. Experiments using paired and flickering stimuli indicated that the high thresholds corresponded to that of cone photoreceptors. In the KO mouse, on-center ganglion cells with low thresholds were completely lost. All on-center cells in the KO mouse showed intensity-response functions similar to those of high threshold cells in WT animals. In contrast, off-center ganglion cells with both low and high thresholds were maintained in the retinas of Cx36 KO mice. However, on average, we found an approximate 0.5 log unit loss in sensitivity across the entire population of off-center ganglion cells. Application of AP4 had no effect on the intensity-response function of off-center ganglion cells in WT mice. However, AP4 shifted the intensity-response functions of all off-center cells in the KO mouse to high (cone) threshold levels. Conclusions: Loss of the gap junctions of AII amacrine cells causes a profound change in the sensitivity of ganglion cells in the mouse retina. The loss of junctions between AII cells and on-center cone bipolars produced a complete loss of rod-mediated on-center responses. In addition, the loss of sensitivity of off-center ganglion cells in the KO mouse suggests that AII-AII cell coupling helps to preserve sensitivity of the rod pathways in proximal retina. Experiments with AP4 suggest a loss of an outer retinal rod pathway in the Cx36 KO mouse, possibly a loss of photoreceptor coupling.

Keywords: 416 gap junctions/coupling • 312 amacrine cells • 557 retina: proximal(bipolar, amacrine, and ganglion cells) 

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