Chenanke Sun¹, Joseph McGuire¹, Janneke Jehee², Sam Ling¹; ¹Boston University, ²Donders Institute for Brain, Cognition and Behavior

Arousal significantly shapes human behavior and sensory processing. Its effects are believed to extend to early visual processing stages, such as contrast sensitivity and spatial frequency processing. Yet, the neural mechanisms underlying these effects remain poorly understood. In this study, we used fMRI to assess how arousal, specifically emotional arousal, modulates population receptive field (pRF) properties in human visual cortex. We combined classic pRF mapping paradigm with auditory cues that varied in its emotional valence (Neutral or Negative valence), drawn from the International Affective Digitized Sounds database (IADS). pRFs were estimated using classical moving bar, wedge, and ring apertures filled with images of objects and faces, while participants were asked to maintain fixation and detect color changes of a central fixation point. During the task, participants heard concatenated negative valence (e.g. people screaming) or neutral (e.g. footsteps) auditory clips from the IADS database, or no auditory stimulus. We estimated pRFs in early visual areas (V1–V3) and compared pRF sizes across auditory conditions, as a function of eccentricity. We found substantially smaller receptive field sizes when participants heard the negative valence stimuli compared to neutral stimuli, with the smallest receptive fields observed in the no-sound condition. This modulation of pRF size was robust across early visual areas V1-V3, and showed a clear eccentricity dependence: differences between conditions were most pronounced in the periphery, with little-to-no modulation at central eccentricities. Together, these results demonstrate that emotional arousal and the presence of auditory input sharpens spatial representations in periphery in early visual cortex, offering new insight into how affective states alter early stages of human visual processing.

Acknowledgements: This work was funded by the National Institutes of Health (NIH) Grand R01EY035640 to S. Ling.