Details

Autor(en) / Beteiligte

• Owen, Scott F.
• Berke, Joshua D.
• Kreitzer, Anatol C.

Titel

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

Ist Teil von

• Cell, 2018-02, Vol.172 (4), p.683-695.e15

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2018

Quelle

MEDLINE

Beschreibungen/Notizen

• 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). In vivo 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 feedforward inhibition from FSIs temporally restricts MSN bursting and calcium-dependent synaptic plasticity to facilitate striatum-dependent sequence learning. [Display omitted] •Fast-spiking interneurons (FSIs) mediate feedforward control of bursting•Feedforward control of bursting restricts calcium entry and plasticity•Restricting plasticity in striatal principal cells facilitates sequence learning•Data suggest a unified model for FSI function in gain control and plasticity Fast-spiking interneurons of the striatum mediate feedforward control of bursting, and their disruption affects learning, but not performance, of striatum-dependent action selection.