October 02, 2017 16:00 - 17:30
BSI Central Building 1F Seminar Room
Fast-spiking interneurons (FSIs) are a prominent class of forebrain GABAergic cells considered essential for regulation of input gain and spike timing. However, their role in learning and network plasticity is less clear. Using optogenetic silencing, we demonstrate that FSIs are the primary source of feed-forward inhibition onto striatal medium spiny projection neurons (MSNs) and tonically inhibit MSN spiking. FSI silencing increased MSN bursting and calcium transients in vivo, highlighting the potential of FSIs to control calcium-dependent plasticity during learning.
In a spatial learning task, FSI silencing increased the overall frequency of calcium transients throughout the task, but reduced the specificity with which calcium 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 limits MSN bursting and restricts calcium-dependent synaptic plasticity to behaviorally-relevant ensembles to facilitate efficient learning.
- Open to Public
- Joshua Johansen [Joshua Johansen, Neural Circuitry of Memory ]