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Cameron Cowan, Meike van der Heijden, Eric Lo, David Paul, Janis Lem, Debra Bramblett, Samuel Wu; The luminal and spatiotemporal dependence of mouse optokinetic contrast sensitivity on rod pathway components. Invest. Ophthalmol. Vis. Sci. 2013;54(15):6147.
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© ARVO (1962-2015); The Authors (2016-present)
Recent studies have exploited the optokinetic image tracking reflex to quantitatively estimate the functional limits of mouse vision. We have improved upon and applied these methods to study knockouts which lack critical components of rod pathways. Mammalian rod pathways converge information from up to hundreds of rods, increasing light sensitivity but reducing spatial acuity. The goal of this project is to determine the contributions of important rod pathway components to the spatiotemporal dependence of contrast sensitivity at different light adaptation states. To accomplish this we studied knockout mice which lack critical components of rod pathways.
Three strains of knockout mice were used: Transducin-α -/- lack rod light responses, Bhlhb4 -/- lack rod bipolar cells, and Cx-36 -/- lack the connexin-36 gap junction which connects AII amacrine cells to cone DBCs. Optokinetic reflexes were measured by placing mice on a platform surrounded by monitors. Stimuli were sinusoidal contrast gratings whose spatiotemporal frequencies, light intensities, and contrasts were varied systematically.
Contrast sensitivity of C57Bl/6J mice was tuned to spatiotemporal frequency, and scotopic responses were shifted to lower spatial and temporal frequencies. Bhlhb4 -/- mice had decreased photopic and scotopic contrast sensitivity compared to WT, but there was no interaction effect between light and other parameters. Tr-α -/- mice lacked all light sensitivity at scotopic intensities, but had weaker light responses than matched controls in photopic conditions. Cx-36 knockouts were statistically unchanged in scotopic conditions, but showed a marked sensitivity increase in photopic compared to WT.
Scotopic shifts toward low spatiotemporal frequencies is consistent with slow rod responses and high rod pathway convergence. Responses in Bhlhb4 knockouts had weakened but surprisingly normal spatiotemporal dependence, which we ascribe to cone DBC driven activation of AII Amacrine cells. The Cx-36 knockouts had increased contrast sensitivity in photopic conditions, which we hypothesize is due to decreased cone DBC input impedance due to loss of AII->cDBC coupling. This project directly informs our understanding of the roles these components play in forming optokinetic responses, and provides insight into their roles in the in vivo retina.
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