Impact of somatostatin interneurons on interactions between barrels in plasticity induced by whisker deprivation.

The activity of inhibitory interneurons has a profound role in shaping cortical plasticity. Somatostatin-expressing interneurons (SOM-INs) are involved in several aspects of experience-dependent cortical rewiring. We addressed the question of the barrel cortex SOM-IN engagement in plasticity formation induced by sensory deprivation in adult mice (2-3 months old). We used a spared vibrissa paradigm, resulting in a massive sensory map reorganization. Using chemogenetic manipulation, the activity of barrel cortex SOM-INs was blocked or activated by continuous clozapine N-oxide (CNO) administration during one-week-long deprivation. To visualize the deprivation-induced plasticity, [14C]-2-deoxyglucose mapping of cortical functional representation of the spared whisker was performed at the end of the deprivation. The plasticity was manifested as an extension of cortical activation in response to spared vibrissae stimulation. We found that SOM-IN inhibition in the cortical column of the spared whisker did not influence the areal extent of the cortex activated by the spared whisker. However, blocking the activity of SOM-INs in the deprived column, adjacent to the spared one, decreased the plasticity of the spared whisker representation. SOM-IN activation did not affect plasticity. These data show that SOM-IN activity is part of cortical circuitry that affects interbarrel interactions underlying deprivation-induced plasticity in adult mice.

Learning-induced plasticity in the barrel cortex is disrupted by inhibition of layer 4 somatostatin-containing interneurons.

Gaba-ergic neurons are a diverse cell class with extensive influence over cortical processing, but their role in experience-dependent plasticity is not completely understood. Here we addressed the role of cortical somatostatin- (SOM-INs) and vasoactive intestinal polypeptide- (VIP-INs) containing interneurons in a Pavlovian conditioning where stimulation of the vibrissae is used as a conditioned stimulus and tail shock as unconditioned one. This procedure induces a plastic change observed as an enlargement of the cortical functional representation of vibrissae activated during conditioning. Using layer-targeted, cell-selective DREADD transductions, we examined the involvement of SOM-INs and VIP-INs activity in learning-related plastic changes. Under optical recordings, we injected DREADD-expressing vectors into layer IV (L4) barrels or layer II/III (L2/3) areas corresponding to the activated vibrissae. The activity of the interneurons was modulated during all conditioning sessions, and functional 2-deoxyglucose (2DG) maps were obtained 24 h after the last session. In mice with L4 but not L2/3 SOM-INs suppressed during conditioning, the plastic change of whisker representation was absent. The behavioral effect of conditioning was disturbed. Both L4 SOM-INs excitation and L2/3 VIP-INs inhibition during conditioning did not affect the plasticity or the conditioned response. We found the activity of L4 SOM-INs is indispensable in the formation of learning-induced plastic change. We propose that L4 SOM-INs may provide disinhibition by blocking L4 parvalbumin interneurons, allowing a flow of information into upper cortical layers during learning.