Author:

Abstract:

The visual cortex of adult mice retains the ability to recover upon deactivation after monocular enucleation (ME). Open eye potentiation induces an early but restricted reactivation, leading to the expansion of the binocular zone into monocular territory. The slower and larger impact of cross-modal plasticity facilitates reactivation of the medial monocular cortex by whisker-related inputs (Van Brussel et al., 2011). A dark exposure (DE) period of 10 days prior to ME specifically prevents the late cross-modal reactivation. DE affects GABAergic synaptic transmission differently in binocular and monocular V1, showing that intracortical inhibition is an important regulator of the cross-modal response to unilateral visual deprivation (Huang et al., 2010; Nys et al., in revision). The subpopulation of somatostatin (SOM)-expressing inhibitory interneurons has the potential to play a role in regulating this cross-modal plasticity. These cells do not receive thalamic input and are widespread in infragranular layers where the cross-modal component has a maximal influence in the visual cortex upon loss of the dominant sensory input (Iurilli et al., 2012; Markram et al., 2004; Urban-Clecko et al., 2015, Van Brussel et al, 2011). Localized optogenetic SOM-interneuron activation in V1/V2M upon Cre-dependent rAAV2/7 driven stable-step function opsin (SSFO) transduction was performed on 3 consecutive days, prior to ME, combined or not with DE pretreatment. Successful activation/deactivation of the SSFOs by blue/yellow laser pulses was verified by means of extracellular multi-unit recordings. The limitation or potentiation of plasticity by optogenetic stimulation of SOM-interneurons was determined by charting the expression levels of the activity marker zif268. The modulation of SOM-interneurons hampered cross-modal plasticity in all conditions. These observations identify the SOM interneuron population as an essential cellular component and call for future investigations aiming at elucidating how SOM-specific inhibitory mechanisms direct cross-modal plasticity in adulthood.