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

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AbstractThe 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.
Title: Impact of somatostatin interneurons on interactions between barrels in plasticity induced by whisker deprivation
Description:
AbstractThe 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.

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