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M. C. Mauck, A. Salzwedel, J. Kuchenbecker, C. Pawela, J. Garcia, J. Hyde, A. Hudetz, T. B. Connor, Jr., J. Neitz, M. Neitz; Probing Neural Circuitry for Blue-Yellow Color Vision Using High Resolution Functional Magnetic Resonance Imaging. Invest. Ophthalmol. Vis. Sci. 2008;49(13):3251.
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There are no models in which to probe mechanisms of human red-green color vision except nonhuman primates. However, other mammals can be studied to understand blue-yellow color vision circuitry. Rats, which fit in the small bore of an ultra high field strength MRI scanner have subcortical brain structures of a favorable size relative to neocortex which together with the scanner’s high spatial resolution (ca. 0.1 X 0.1 mm voxels; in 1 mm slices) allows visualization of color vision circuit activity throughout the CNS. A distinct pathway assumed to be a substrate for blue-yellow color vision has been traced in primates from depolarizing S-cone bipolar cells to small bistratified ganglion cells to LGN koniocellular layers to VI layers 2/3. Blood oxygenation level dependent (BOLD) signals were obtained in response to heterochromatically modulated S-(max = 360 nm) and M-cone isolating stimuli from rats in which the S-cone bipolar pathway was blocked in one hemisphere via monocular injection of 2-amino-4-phosphonobutyrate (APB); this also blocked input to "S-OFF" melanopsin ganglion cells, the other well characterized cell type carrying S cone input.
Lights were delivered to anesthetized rats in a 9.4T MRI system through fiber optics to provide full field, diffuse illumination binocularly. 5 rats received an intravitreal injection of 2-APB monocularly.
In the hemisphere receiving input from the untreated eye, S-cone stimuli activated the dorsal and ventral lateral geniculate nucleus (dLGN & vLGN). As expected, subcortical BOLD signals in response to S-cone stimuli were greatly reduced on the APB treated side. The absence of signal to the vLGN is presumably the result of melanopsin ganglion cell blockade, while the diminished dLGN response reflects the obstruction of the S-cone bipolar pathway. Stunningly, in contrast to the pattern of subcortical activation, the BOLD signals were dramatically enhanced in neocortex in response to S-cone isolating stimuli presented to the APB treated eye.
The pathway which has been assumed to be responsible for blue-yellow color vision actually undergoes a sign-reversal at the level of the cortex damping responses to S-cone stimuli. Excitatory S-cone signals must be derived from a pathway that originates from hyperpolarizing bipolar cells. Thus, two S-cone pathways one originating from hyperpolarizing and the other from depolarizing bipolar cells are likely to provide the antagonistic components of S+/S- receptive fields proposed from psychophysics.
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