April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Gain Control At Rod Bipolar Cell Synapses Is Driven Primarily By Vesicle Depletion
Author Affiliations & Notes
  • Joshua H. Singer
    Northwestern University, Chicago, Illinois
  • Mark Cembrowski
    Applied Math,
    Northwestern University, Chicago, Illinois
  • Stephen Logan
    Northwestern University, Chicago, Illinois
  • Jonathan Demb
    Ophthalmology, University of Michigan, Ann Arbor, Michigan
  • Tim Jarsky
    Northwestern University, Chicago, Illinois
  • Footnotes
    Commercial Relationships  Joshua H. Singer, None; Mark Cembrowski, None; Stephen Logan, None; Jonathan Demb, None; Tim Jarsky, None
  • Footnotes
    Support  NIH Grants EY017836, EY021372
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 4806. doi:
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      Joshua H. Singer, Mark Cembrowski, Stephen Logan, Jonathan Demb, Tim Jarsky; Gain Control At Rod Bipolar Cell Synapses Is Driven Primarily By Vesicle Depletion. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4806.

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

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Purpose: : The visual system continually adapts its sensitivity, or gain, to encode a wide range of mean luminance and contrast levels with a narrow range of neuronal output signals. Consequently, multiple adaptive mechanisms are required to adjust the receptive field properties of retinal neurons to the statistics of the visual scene. An important known site of gain control during rod-mediated (i.e., night, or scotopic) vision in mammals is the synapse between rod bipolar (RB) and AII amacrine cells. Here, we describe a synaptic mechanism that permits the gain of individual RB synapses to be adjusted independently as the number of photon absorptions by presynaptic rods increases. This mechanism provides a means by which adaptation to mean intensity and contrast can be achieved at the level of individual synapses.

Methods: : Whole-cell voltage-clamp recordings were made at near-physiological temperatures (33-35 °C) from rod bipolar and AII amacrine cells in mouse retinal slices (P25-35; 200 µm thick).

Results: : We determined how changes in RB membrane potential similar to those that are induced by varying the mean luminance of a visual scene affect the gain of signal transfer to AIIs. We did this by making paired, voltage-clamp recordings from presynaptic RBs and postsynaptic AIIs in a mouse retinal slice preparation and simulating changes in mean luminance and local contrast by adjusting the mean and variance of a quasi-white noise stimulus delivered to a presynaptic RB. We employed a simple analytical approach derived from linear systems analysis to quantify voltage-dependent changes in the gain of the RB-AII synapse.

Conclusions: : Our analysis indicated that the gain of transmission is reduced substantially by tonic presynaptic activity designed to mimic RBs’ responses to increased mean luminance and contrast. A linear systems analysis of paired-cell recordings showed that steady bipolar cell depolarization reduced synaptic gain by ~50%. Reduced gain depended partially on presynaptic calcium channel inactivation but primarily on vesicle depletion. The rod bipolar synapse also adapted to increased variance in membrane potential, reducing its gain by ~20%. Vesicle depletion generates adaptation to both the mean and variance of bipolar cell membrane potential and enables each cell to control output gain independently. This notion was confirmed using a realistic simulation of synaptic transmission.

Keywords: bipolar cells • amacrine cells • synapse 

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