fMRI signals arise from interactions among multiple cell types, complicating their interpretation. While excitatory neurons are often considered primary drivers, inhibitory neurons and astrocytes also modulate hemodynamic responses but remain less explored. We show that somatostatin-expressing (SST) inhibitory neurons generate delayed fMRI signals via an SST–astrocyte pathway. These responses were slower, broader, and localized to cortical input layers, providing a cellular basis for laminar-specific fMRI. Our findings reveal a critical role for inhibitory neurons and astrocytes in shaping fMRI dynamics and emphasize the need for a network-level framework to interpret high-resolution fMRI.
Vo et al. (Mon,) studied this question.