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要旨

We characterized eccentricity variation in the temporal sensitivity of human primary visual cortex (V1) to flicker that targeted the post-receptoral channels (luminance, red-green, blue-yellow). These responses were modeled as a transformation of the signals that arise in the different classes of retinal ganglion cells (RGCs). We measured 7T BOLD fMRI from two participants viewing a high-contrast, flickering, wide (~150°) uniform field. Stimulus frequency varied logarithmically between 2 and 64 Hz and targeted L+M+S, L-M, and S-[L+M] cone combinations. We obtained the average LGN response, and V1 responses across eccentricity bands. These data were fit with a temporal sensitivity model based on electrophysiologic responses of macaque midget, parasol, and bistratified RGCs to chromatic and achromatic flicker at multiple eccentricities (Yeh et al. 1995; Solomon et al. 2002, 2005). Low pass filtering, surround inhibition, and multiplicative gain were applied to the fixed RGC responses to fit the LGN and V1 data. Model comparison and inference were accomplished by fitting across bootstrap resampling of the imaging acquisitions. fMRI responses reflected known properties of the visual system, including higher peak temporal sensitivity to achromatic vs. chromatic stimuli, and low-pass filtering between LGN and V1. Peak temporal sensitivity decreased at greater V1 eccentricities, a finding not predicted by retinal responses. A model that accounted for these data in terms of RGC signals had the following elements: 1) low pass filtering between the retina and LGN, and between the LGN and cortex, 2) delayed surround suppression applied to LGN and V1 responses pooled by post-receptoral channel, strongest at the fovea and weaker towards the periphery, and 3) multiplicative gain that amplified retinal signals at low eccentricities for blue-yellow ~10x as compared to luminance, and ~10x for luminance compared to red-green. Delayed surround suppression helps explain differences in flicker temporal sensitivity between RGCs and V1.