Emotional arousal modulates the gain of contrast responses in human LGN

Poster Presentation: Saturday, May 17, 2025, 2:45 – 6:45 pm, Pavilion
Session: Attention: Neural, spatial

Chenanke Sun1 (), Jasmine Pan1, Louis Vinke3, Joseph McGuire1, Janneke Jehee2, Sam Ling1; 1Boston University, 2Donders Institute for Brain, Cognition and Behavior, 3Massachusetts General Hospital

Arousal is known to play a significant role in human behavioral performance and sensory processing. While its influence is believed extends to early vision, including as contrast sensitivity and spatial frequency processing, the neural mechanisms that give rise to these effects remain a poorly understood. To shed light on emotion’s effects on vision, in this study we leveraged fMRI to assess how emotional arousal modulates the gain of the population contrast response function (CRF) in human visual processing. To do so, we measured BOLD CRFs within a participant’s early visual cortex (V1-V3) and lateral geniculate nucleus (LGN), while they concurrently listened to auditory clips that were emotionally charged. To homogenize the population CRF, participants underwent a contrast adaptation paradigm, adapting to gratings of a fixed contrast level (16%) before viewing gratings with parametrically varied contrast levels (9 contrast levels, 2.67-96%). This paradigm was accompanied by sounds that were Negative or Neutral valence, taken from the International Affective Digitized Sounds (IADS) database. We found substantial increases in the response of the amygdala when participants heard the negative valence stimuli, supporting the efficacy of these stimuli. Interestingly, we discovered substantial changes in the CRFs within the LGN, but there were little-to-no modulatory effects of emotional arousal on the CRF in visual cortex. Specifically, we found an increase in the baseline response of the CRF in the LGN when participants listened to negative sounds compared to neutral sounds. Taken together, these findings suggest that emotional processing takes a predominantly subcortical route.

Acknowledgements: NIH RO1 EY035640; NIH RO1 EY028163