Optogenetic Activation of Interneuron Subtypes Modulates Visual Contrast Responses of Mouse V1 Neurons.

Interneurons are critical for information processing in the cortex. In vitro optogenetic studies in mouse primary visual cortex (V1) have sketched the connectivity of a local neural circuit comprising excitatory pyramidal neurons and distinct interneuron subtypes that express parvalbumin (Pvalb+), somatostatin (SOM+), or vasoactive intestinal peptide (VIP+). However, in vivo studies focusing on V1 orientation tuning have ascribed discrepant computational roles to specific interneuron subtypes. Here, we sought to clarify the differences between interneuron subtypes by examining the effects of optogenetic activation of Pvalb+, SOM+, or VIP+ interneurons on contrast tuning of V1 neurons while also accounting for cortical depth and photostimulation intensity. We found that illumination of the cortical surface produced a similar spectrum of saturating additive photostimulation effects in all 3 interneuron subtypes, which varied with cortical depth rather than light intensity in Pvalb+ and SOM+ cells. Pyramidal cell modulation was well explained by a conductance-based model that incorporated these interneuron photostimulation effects.

Activating parvalbumin-expressing interneurons produces iceberg effects in mouse primary visual cortex neurons.

In the primary visual cortex (V1) inhibitory interneurons form a local circuit with excitatory pyramidal cells to produce distinct receptive field properties. Parvalbumin-expressing interneurons (Pvalb+) are the most common subclass of V1 interneurons, and studies of orientation tuning indicate they shape pyramidal stimulus selectivity by balancing excitation with inhibition relative to the spike threshold. The iceberg effect, where subthreshold responses have broader tuning than spiking responses, predicts that other receptive field properties besides orientation tuning should also be affected by this balance mediated by Pvalb+ cells. To test this, we measured receptive field size and visual latency of pyramidal cells while Pvalb+ activity was optogenetically increased. We found that amplifying Pvalb+ input to pyramidal cells significantly increased their latency and decreased their receptive field size, which corroborates the proposed role of Pvalb+ interneurons in sculpting pyramidal tuning by controlling cortical gain.