Early suppressive mechanisms and the negative blood oxygenation level-dependent response in human visual cortex

Abstract

Functional magnetic resonance imaging (fMRI) studies of early sensory cortex often measure stimulus-driven increases in the blood oxygenation level-dependent (BOLD) signal. However, these positive responses are frequently accompanied by reductions in the BOLD signal in adjacent regions of cortex. Although this negative BOLD response (NBR) is thought to result from neuronal suppression, the precise relationship between local activity, suppression, and perception remains unknown. By measuring BOLD signals in human primary visual cortex while varying the baseline contrast levelsinthe region affected bythe NBR, we tested three physiologically plausible computational models of neuronal modulation that could explain this phenomenon: a subtractive model, a response gain model, and a contrast gain model. We also measured the ability of isoluminant contrast togeneratean NBR. Weshow that the NBR can bemodeled as a pathway-specific contrast gain modulation thatis strongest outside the fovea.We foundasimilar spatial biasina psychophysical study usingidentical stimuli, although these dataindicatedaresponse gainrather thanacontrast gain mechanism.Wereconcile these findings by proposing (1) that the NBR is associated with a long-range suppressive mechanism that hyperpolarizes a subset of magnocellularly driven neurons atthe input to V1, (2) that this suppressionis broadly tuned tomatch the spatial features of the mask region, and (3) that increasing the baseline contrast in the suppressed region drives all neurons in the input layer, reducing the relative contribution of the suppressing subpopulation in the fMRI signal. Copyright © 2010 the authors.