March 2012
Volume 53, Issue 14
Free
ARVO Annual Meeting Abstract  |   March 2012
Differences in GABA Receptor Contribution to Surround Inhibition Between the ON and OFF Pathways in the Mammalian Retina
Author Affiliations & Notes
  • Ilya Buldyrev
    Casey Eye Institute, Oregon Health & Science University, Portland, Oregon
  • W. Rowland Taylor
    Casey Eye Institute, Oregon Health & Science University, Portland, Oregon
  • Footnotes
    Commercial Relationships  Ilya Buldyrev, None; W. Rowland Taylor, None
  • Footnotes
    Support  EY014888
Investigative Ophthalmology & Visual Science March 2012, Vol.53, 5375. doi:
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      Ilya Buldyrev, W. Rowland Taylor; Differences in GABA Receptor Contribution to Surround Inhibition Between the ON and OFF Pathways in the Mammalian Retina. Invest. Ophthalmol. Vis. Sci. 2012;53(14):5375.

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Abstract

Purpose: : Most retinal ganglion cells display concentric, centre-surround receptive fields, which increase sensitivity to contrast borders. Amacrine cells in the inner-plexiform layer are thought to contribute to surround suppression, however, the relative role of the different GABA receptors remains uncertain.Here we investigated the role of GABAergic transmission in providing surround inhibition to the ON and the OFF pathways, using the ON and OFF brisk-sustained ganglion cells (BSGCs) in the rabbit retina.

Methods: : Extracellular and whole-cell voltage clamp recordings were performed in whole-mount retinal preparations at 36 C. Spot stimuli of variable diameter were centered in the BSGC receptive field. The spot intensity was square-wave modulated at 1Hz with a peak-to-peak amplitude of 20% relative to a photopic background. The strength of surround inhibition was determined by modeling the stimulus size-response function as a difference of Gaussian integrals.

Results: : Our recordings demonstrate that most of the GABAergic portion of surround inhibition is presynaptic to the BSGCs, suppressing both excitatory inputs from bipolar cells and inhibitory inputs from narrow-field glycinergic amacrine cells. Extracellular recordings showed that this presynaptic inhibition almost completely suppressed stimulus-evoked spike output in both ON (96 ± 2.3%) and OFF (98 ± 2.0%) BSGCs. However, in the presence of GABA blockers, surround stimulation suppressed responses by 61±10% in ON and 57±3% in OFF BSGCs. The residual surround inhibition likely originates in the outer plexiform layer. In ON BSGCs, signaling via GABAC receptors was sufficient to account for the GABAergic surround suppression. However, in OFF BSGCs, blocking both GABAA and GABAC receptors was required to significantly increase the spike output and synaptic excitation in response to wide-field stimuli. Although large spots activated a small, GABAA receptor-mediated feed-forward inhibitory input in OFF BSGCs, selectively blocking GABAA receptors did not increase OFF BSGC responsiveness to wide-field stimuli, indicating that postsynaptic inhibition did not play a major role in generating the surround.

Conclusions: : Although GABAA receptors contribute to surround inhibition in OFF BSGCs our results suggest that, GABAC receptor signaling at bipolar cell terminals is central to surround inhibition in both the OFF and ON pathways.

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