Abstract

Neuronal activity evokes a vascular response that is essential to sustain brain function. We show that neurovascular coupling (NVC) is mediated by long-range projecting GABAergic neurons that express Tacr1. Whisker stimulation elicited Tacr1 neuron activity in the barrel cortex through feed-forward excitatory pathways. Optogenetic activation of Tacr1 neurons elicited vasodilation, whereas inhibition significantly reduced whisker-evoked hemodynamic responses. Moreover, vasodilation was preceded by capillary pericyte activity, demonstrating a mechanism for NVC.