The role of interneurons in sensory processing in primary visual cortex

Cortical networks are comprised of a multitude of cell types. To understand sensory processing, the function and interaction of these cell types must be investigated. Neurons can be separated into two main groups: excitatory pyramidal (Pyr) cells and inhibitory interneurons. Inhibitory interneurons make up 20% of the total cortical neuronal population and they exhibit a striking array of molecular, morphological and electrophysiological characteristics. The most numerous are the parvalbumin-expressing (PV+) interneurons, accounting for 35-40% of the interneuron population in adult mouse visual cortex. Somatostatin-expressing (SOM+) neurons are another significant group, comprising 20-25% of the interneuron population. The visual responses of SOM+ and PV+ interneurons were measured using 2-photon targeted cell-attached recordings and compared with Pyr cells in the primary visual cortex of anaesthetized mice. These interneuron populations exhibited higher firing rates than Pyr cells in response to oriented gratings, but were less orientation selective, with PV+ interneurons exhibiting the lowest orientation selectivity. Next, SOM+ interneurons were stimulated optogenetically using channelrhodopsin to measure their effect on Pyr cell and PV+ interneuron responses to visual stimuli. Activating small numbers of SOM+ interneurons in vivo inhibited stimulus- evoked firing in PV+ interneurons but not in Pyr cells. Stimulating a large number of SOM+ interneurons confirmed this differential effect, inhibiting PV+ interneurons twice as effectively as Pyr cells. Moreover, the remaining responses to oriented gratings in PV+ cells were more orientation-tuned and time-modulated. In short, inhibitory SOM+ cell activity does not summate with PV+ cell activity, but suppresses it, reconfiguring the inhibitory input to Pyr cells. These results suggest a new role for SOM+ cells, which are activated more slowly and provide dendritic inhibition to Pyr cells while strongly antagonizing PV+ cells, thereby shifting inhibitory input to Pyr cells from somatic to dendritic inhibition throughout the course of the network's visual response