Neural circuits of the primary visual cortex (V1) are critical for generating perceptions of our external world. In V1, most neurons exhibit potent modulation by stimuli that are outside their receptive fields, a process termed ?surround modulation?. Importantly, the magnitude and sign of surround modulation depend on the orientation and contrast of the center and surround ? leading to the notion that flexible surround modulation contributes to scene segmentation, salience detection, contour integration, and figure/ground segregation. The specific neural circuits in V1 that explain the feature dependence of surround modulation are largely unknown. By combining intracellular and extracellular electrophysiology, two photon imaging, and optogenetics in awake mice, we aim to reveal the inhibitory circuits in V1 that can account for these fundamental features of V1 computation. Specifically, we will test the hypothesis that a competitive inhibitory interaction between two types of V1 GABAergic interneurons (?SST? and ?VIP?) cells, provides a circuit and synaptic basis for the feature dependence of surround modulation. We will image the visual responses of these two subtypes, then manipulate them optogenetically while recording neural activity extracellularly, or synaptic currents intracellularly, to test whether their visual responses and network impact are consistent with key roles in the orientation and contrast dependence of surround modulation. These experiments will provide critical new insight into how cortical inhibitory circuits mediate key aspects of sensory perception.
How excitatory and inhibitory circuits mediate neural computation in the cerebral cortex is central to understanding vision, and brain function more generally. Disruptions of the precise balance between excitation and inhibition in the cerebral cortex can lead to a variety of neurological disorders. Thus, understanding how excitatory and inhibitory circuits drive sensory perception should help reveal the underlying causes of certain neurological diseases.