May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
Push-Pull Modulation of Ganglion Cell Light Response in the Inner Plexiform Layer of Mouse Retina
Author Affiliations & Notes
  • Y. Xia
    Ophthalmology and Visual Science, and Neuroscience, Albert Einstein College of Med, Bronx, NY, United States
  • S. Nawy
    Ophthalmology and Visual Science, and Neuroscience, Albert Einstein College of Med, Bronx, NY, United States
  • Footnotes
    Commercial Relationships  Y. Xia, None; S. Nawy, None.
  • Footnotes
    Support  NIH Grant EY10254
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 2068. doi:
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      Y. Xia, S. Nawy; Push-Pull Modulation of Ganglion Cell Light Response in the Inner Plexiform Layer of Mouse Retina . Invest. Ophthalmol. Vis. Sci. 2003;44(13):2068.

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

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Abstract

Abstract: : Purpose: In cold-blooded vertebrates, there is strong physiological evidence for push-pull regulation of ganglion cell light responses by the ON and OFF pathways (Belgum et al, 1982; 1983; 1984). In this abstract, we report evidence that a similar arrangement exists in the mouse retina. Methods: C57/BL6 mouse retina was dissected in dim red light, mounted in the recording chamber with the ganglion cell layer facing up and superfused with Ames media. Whole-cell recordings from ganglion cells were obtained by severing the upper limiting membrane of the Müller cell endfeet to get access to ganglion cells. Light stimulation was focused through the 40x objective via a camera port onto the retina and turned on for 1 sec once every 30 sec. Results: To look for synaptic input from the ON pathway, we applied 300 µM CPPG, an mGluR6 antagonist, in the bath. CPPG depolarizes ON bipolar cells by opening mGluR6-gated cation channels. Using voltage steps, we measured the I-V relations of OFF ganglion cells in darkness, and during the presentation of light. CPPG increased membrane conductance in darkness. This conductance was due to an increase in a current that reversed near –50 mV, close to ECl- in our recordings. Ordinarily this input is transient, observed only during light stimulation, but CPPG, which tonically depolarizes ON bipolar cells, converted this into a sustained inhibition. For ON ganglion cells, CPPG blocked the excitatory component of the light response as expected. In darkness, it also increased the frequency of discreet, spontaneous events, which might be due to an increase in quantal release from ON bipolar cells that have been depolarized by CPPG. I-V relations measured in ON ganglion cells suggested that ON bipolar also inhibit ON ganglion cells via an intervening amacrine cell, but the magnitude of this inhibition is much smaller in ON ganglion cells than in OFF cells. Conclusions: By using CPPG to antagonize synaptic transmission at the ON bipolar cell we provide evidence that ON bipolar cells strongly inhibit cells in the OFF pathway via an intermediate amacrine cell.

Keywords: ganglion cells • retina: proximal(bipolar, amacrine, and gangli • retinal connections, networks, circuitry 
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