RT Journal Article
SR Electronic
T1 Saccadic Suppression of Retinotopically Localized Blood Oxygen Level-Dependent Responses in Human Primary Visual Area V1
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 5965
OP 5969
DO 10.1523/JNEUROSCI.0817-06.2006
VO 26
IS 22
A1 Ignacio Vallines
A1 Mark W. Greenlee
YR 2006
UL http://www.jneurosci.org/content/26/22/5965.abstract
AB Saccadic eye movements are responsible for bringing relevant parts of the visual field onto the fovea for detailed analysis. Because the retina is physiologically unable to deliver sharp images at very high transsaccadic speeds, the visual system minimizes the repercussion of the blurry images we would otherwise perceive during transsaccadic vision by reducing general visual sensitivity and increasing the detection threshold for visual stimuli. Ruling out a pure retinal origin, the effects of saccadic suppression can be already observed some 75 ms before the onset of a saccadic eye movement and are maximal at the onset of motion. The perception of a briefly presented stimulus immediately before the onset of any retinal motion is thus impaired despite the fact that this stimulus is projected onto the stationary retina and is, therefore, physically identical to that presented when no saccadic programming is in course. In this functional magnetic resonance imaging event-related study, we flashed Gabor patches at different times before the onset of a horizontal saccade and measured blood oxygen level-dependent responses at their encoding regions in primary visual cortex (V1) while subjects judged the relative orientation of the stimuli. Closely matching the significant reduction in behavioral performance, the amplitude of the responses in V1 consistently decreased as the stimuli were presented closer to the saccadic onset. These results demonstrate that the neural processes underlying saccade programming transiently modulate cortical responses to briefly presented visual stimuli in areas as early a V1, providing additional evidence for the existence of an active saccadic suppression mechanism in humans.