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      Fast-Spiking Interneurons Supply Feedforward Control of Bursting, Calcium, and Plasticity for Efficient Learning

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      Cell
      Elsevier BV

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          Abstract

          <p id="P3">Fast-spiking interneurons (FSIs) are a prominent class of forebrain GABAergic cells implicated in two seemingly independent network functions: gain control and network plasticity. Little is known, however, about how these roles interact. Here, we use a combination of cell-type-specific ablation, optogenetics, electrophysiology, imaging, and behavior to describe a unified mechanism by which striatal FSIs control burst firing, calcium influx, and synaptic plasticity in neighboring medium spiny projection neurons (MSNs). <i>In vivo</i> silencing of FSIs increased bursting, calcium transients, and AMPA/NMDA ratios in MSNs. In a motor sequence task, FSI silencing increased the frequency of calcium transients, but reduced the specificity with which transients aligned to individual task events. Consistent with this, ablation of FSIs disrupted the acquisition of striatum-dependent egocentric learning strategies. Together, our data support a model in which feed-forward inhibition from FSIs temporally restricts MSN bursting and calcium-dependent synaptic plasticity to facilitate striatum-dependent sequence learning. </p><p id="P4">Fast-spiking interneurons of the striatum mediate feed-forward control of bursting, and their disruption affects learning but not performance of striatum dependent action selection. </p><p id="P5"> <div class="figure-container so-text-align-c"> <img alt="" class="figure" src="/document_file/b8968bfd-92ac-41e4-8d69-7ce8ff3a4138/PubMedCentral/image/nihms932891u1.jpg"/> </div> </p>

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          Author and article information

          Journal
          Cell
          Cell
          Elsevier BV
          00928674
          February 2018
          February 2018
          : 172
          : 4
          : 683-695.e15
          Article
          10.1016/j.cell.2018.01.005
          5810594
          29425490
          777da531-e368-443c-8672-a586eeb437ef
          © 2018

          http://www.elsevier.com/tdm/userlicense/1.0/

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