Abstract
A natural consequence of executing a saccade is having two separate representations of the target object: pre-saccadic and post-saccadic. To perceive the world as stable, the visual system must integrate these two representations of the saccade target. Previous research suggests that transsaccadic object updating may depend on visual working memory (VWM) processes (Currie et al., 2000; van der Stigchel & Hollingworth, 2018). In the present study, we recorded functional near-infrared spectroscopy (fNIRS) data and tested whether transsaccadic updating is associated with neural signatures of VWM dynamics by disrupting object continuity in a blanking paradigm. Todd and Marois (2004) previously showed that bilateral posterior parietal cortex (PPC) activation increases as the number of items in VWM increases. If disruption of object continuity results in two object representations (pre- and post-saccadic), and if these representations are stored in VWM, then we expect to find a similar increase in PPC activation. On each trial, participants were instructed to execute a saccade to a color disk. On half of the trials, object continuity was disrupted by removing the target from the screen for 250ms after the initiation of the saccade. On some trials the target’s color was also changed by 45° during the saccade. Participants were asked to report the color of either the pre-saccadic or the post-saccadic disk. Preliminary data showed stronger bilateral PPC activation when the target object was blanked compared to when it was not. Moreover, this effect was stronger when the object’s color was also changed. These findings suggest that disrupting the target’s continuity with both blanking and color-change resulted in two separate VWM representations. Additionally, the lack of PPC activation for when stability was not disrupted (no-blank trials) suggests that there was only one VWM representation present, supporting the object-mediated updating account of transsaccadic perception (Tas et al., 2012).
Acknowledgement: This work was supported by NIH R01HD092485 to ATB.