Resting-state EEG alpha-BOLD coupling spatially follows cortical cell-type and receptor gradients

The coupling between electroencephalography (EEG) and blood-oxygen-level-dependent (BOLD) signals has been investigated across numerous studies, but its neurobiological underpinnings remain poorly understood. Resting-state EEG alpha-BOLD coupling follows a characteristic spatial pattern, shifting from negative correlations in sensory regions to positive correlations in association cortices. In this study, we examined neurobiological correlates of resting-state alpha-BOLD coupling. We compared the spatial pattern of the alpha-BOLD coupling map to 82 cortical feature maps, including gene expression profiles of different cell types and receptor subunits as well as structural MRI measures. We identified three statistically significant ( $q<0.05$ FDR-corrected) maps: the layer 6 VIP interneuron marker, excitatory layer-5 marker, and NMDA receptor subunit GRIN2C. The three significant gene maps, combined in a multiple linear regression model, explained $R^2=0.312$ of the spatial variance in alpha-BOLD coupling. Analysis of the spatial mismatch between cortical maps and the alpha-BOLD coupling map revealed that the early auditory cortex is the region that consistently diverges from predictions across gene expression and T1/T2 maps. The spatial correspondence between alpha-BOLD coupling and gene expression profiles of specific receptor subunits, neuronal types, and layer-specific populations identifies these as concrete candidates for future computational and experimental studies of alpha-BOLD coupling.