While sensory environments can vary dramatically in their statistics, neurons have a limited dynamic range with which they can encode sensory information. In sensory cortex, this problem is in part resolved by the systematic adjustment of neural gain in accordance with the contrast of sensory input. This computation also results in contrast invariant representations in cortex that are also more resilient to static background noise. The biophysical basis of contrast gain control (CGC) is currently unknown but shunting inhibition by parvalbumin positive (PV+) interneurons is a likely candidate. We aim to investigate the mechanistic basis of CGC using mice as our model organism, given that optogenetic methods for the circuit level interrogation of the nervous system are well established in that species. First, we characterised CGC in the anaesthetised mouse by performing large scale extracellular recordings across all layers of A1. We found that CGC is present in units recorded in all layers of mouse A1. In order to test the involvement of PV+ interneurons in CGC, we expressed the light-driven neural silencer Archaerhodopsin (Arch) in these cells using a transgenic approach. This allowed us to optogenetically reduce the activity of PV+ interneurons while presenting sensory stimuli that elicit CGC. We find that this manipulation produces a multiplicative disinhibition in pyramidal cell responses, indicative of a change in neuronal gain. This is in keeping with the hypothesis that CGC in pyramidal cells is produced by shunting inhibition provided by contrast driven changes in PV+ activity.