Abstract
Striatal fast spiking interneurons (FSI) modulate the output of the striatum by synchronizing medium-sized spiny neurons (MSN). FSI are the only striatal neurons to express the calcium-binding protein parvalbumin (PV). This selective expression of PV raises questions about the functional role of this calcium buffer in controlling FSI calcium dynamics, and, consequently, the FSI spiking mode and neurotransmission. To study the functional involvement of FSI in striatal microcircuit activity and the role of PV in FSI function, we performed perforated patch recordings on EGFP-expressing FSI in brain slices from control and PV-/- mice. Our results revealed that PV-/- FSI fired more regularly and were more excitable than control FSI by a mechanism in which calcium buffering is linked to spiking activity as the result of the activation of small conductance (SK) calcium-dependent potassium channels. A modeling approach of striatal FSI supports our experimental results. Furthermore, PV deletion modified frequency-specific short-term plasticity at inhibitory FSI to MSN synapses. Our results therefore support the hypothesis that in FSI, PV is crucial for the fine-tuning of the temporal responses of the FSI network and for the orchestration of MSN populations. This, in turn, may play a direct role in the generation and pathology-related worsening of motor rhythms.
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