Primary sensory cortices may be regulated by feedback projections from higher association areas to achieve higher cognitive ability during attentional control. However, the functional and structural bases remain uncertain. To better understand the neural mechanisms underlying the feedback regulation of sensory processing, we investigated the inhibitory controls from the parietal association area to the primary visual cortex (V1) using transcranial flavoprotein fluorescence imaging in mice. Our results revealed that the parietal association area has an ability to negatively regulate the activity of V1: we observed the reduction or the enhancement of the visual responses in V1, when the neural activity in the parietal association area was turned up or down, by electrical stimulation applied to the area or by the lesion, respectively. These effects were not caused by damages or activations of the passing fibers in the area as indicated by the following two experiments. Firstly, inhibition of the parietal association area with muscimol injection resulted in the enhancement of visual responses in V1. Secondly, activation of the area using caged glutamate resulted in the reduction of visual responses in V1. In the latter experiment, the parietal association area injected with MNI-caged-L-glutamate was illuminated using a UV (wave length: 365 nm) flash light source (FLOS-01, Craft Center SAWAKI Inc.) to release glutamate. We observed not only the excitatory activity in the stimulated area but also the decrease in flavoprotein fluorescence signals in V1. We further found that the inhibitory projections from the parietal area to V1 were important for enhancing V1 sensitivity to low contrast grating patterns. Now, we are investigating the responsible neural circuits with tracer injection experiments. Our preliminary results suggest the presence of direct cortico-cortical pathways and indirect pathways via reticular thalamic nucleus, both of which could be responsible for the inhibitory control from the parietal association area to V1.