June 2017
Volume 58, Issue 8
Open Access
ARVO Annual Meeting Abstract  |   June 2017
Different activity patterns in retinal ganglion cells of TRPM1 and mGluR6 knockout mice
Author Affiliations & Notes
  • Chieko Koike
    College of Pharmaceutical Sciences, Ritsumeikan University, Kusatsu, Japan
    Center for Systems Vision Sciences, Ritsumeikan University, Kusatsu, Japan
  • Kanago Taniguchi
    Graduate School of Information Science and Engineering, Ritsumeikan University, Kusatsu, Japan
  • Haruki Takeuchi
    Graduate School of Life Sciences, Ritsumeikan University, Kusatsu, Japan
  • Yasuhiro Tsubo
    College of Information Science and Engineering, Ritsumeikan University, Kusatsu, Japan
    Center for Systems Vision Sciences, Ritsumeikan University, Kusatsu, Japan
  • Katsunori Kitano
    College of Information Science and Engineering, Ritsumeikan University, Kusatsu, Japan
    Center for Systems Vision Sciences, Ritsumeikan University, Kusatsu, Japan
  • Footnotes
    Commercial Relationships   Chieko Koike, None; Kanago Taniguchi, None; Haruki Takeuchi, None; Yasuhiro Tsubo, None; Katsunori Kitano, None
  • Footnotes
    Support  Grant-in-Aid for Scientific Research (B), MEXT-Supported Program for the Strategic Research Foundation at Private Universities
Investigative Ophthalmology & Visual Science June 2017, Vol.58, 231. doi:
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      Chieko Koike, Kanago Taniguchi, Haruki Takeuchi, Yasuhiro Tsubo, Katsunori Kitano; Different activity patterns in retinal ganglion cells of TRPM1 and mGluR6 knockout mice. Invest. Ophthalmol. Vis. Sci. 2017;58(8):231.

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

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Abstract

Purpose : An essential step in visual processing is the segregation of signals into ON and OFF pathways by retinal bipolar cells (BCs). Glutamate released from photoreceptors modulates the photoresponse of ON BCs via metabotropic glutamate receptor 6 (mGluR6) and a G protein (Go) that regulates a cation channel, TRPM1. We examined the ON and OFF responses of retinal ganglion cells (RGC) in TRPM1 and mGluR6 knockout(KO)mice based on the prediction that the deficits in RGC responses would be similar in both cases.

Methods : TRPM1 KO and mGluR6 KO mouse lines were generated by disruption of the TRPM1 or mGluR6 gene by homologous recombination, respectively (Koike et al., 2010, Masu et al., 1995). Spike discharges of RGCs in the isolated mouse retina were recorded by a multielectrode array (60pMEA200-30iR-Ti, MEA-60 system). The retina was stimulated diffusely by a 490 nm light emitting diode (LED; 4.44μW/cm2), 2 s with the light on (9.77μW/cm2) and 2 s with the light off (0.567μW/cm2) in Ringer solution. Data were analyzed by Lab chart and further sorted by Efficient Technology of Spike sorting (EToS4). To analyze retinal circuits, cryosections were subjected to immunohistochemistry and imaged with LSM700 confocal microscope. A computer model was created and simulations were performed.

Results : Significant spontaneous activity was observed in the TRPM1 KO retinas but not in the WT or mGluR6 KO retinas. Spontaneous activity in the TRPM1 KO retina was inhibited by a gap junction inhibitor (MFA). Rod BC terminals in the TRPM1 KO retina were significantly smaller than those in WT or mGluR6 KO retinas. We equated the smaller size of the rod bipolar cell terminals in the TRPM1 KO retina with a decrease in transmitter release. We then used a model to examine the consequences of this morphological changes on the AII-AC network and identified a condition under which oscillations were induced in the network.

Conclusions : Although both TRPM1 and mGluR6 regulate ON bipolar visual transmission, we found a significant difference in spontaneous activity between TRPM1 and mGluR6 KO mouse retinas. The smaller size of the rod bipolar cell terminals in the TRPM1 KO retina, but not in mGluR6 KO retina, are consistent with a decrease in transmitter release altering the AII-AC network to produce oscillations.

This is an abstract that was submitted for the 2017 ARVO Annual Meeting, held in Baltimore, MD, May 7-11, 2017.

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