Parvalbumin tunes spike-timing and efferent short-term plasticity in striatal fast spiking interneurons.

Striatal fast spiking interneurons (FSI) modulate the output of the striatum by synchronizing medium-sized spiny neurons (MSN). Recent studies have broadened our understanding of FSI, showing that they are implicated in severe motor disorders such as Parkinsonism, dystonia and Tourette syndrome. 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 Ca2+ buffer in controlling FSI Ca2+ 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 Ca2+ buffering is linked to spiking activity as the result of the activation of small conductance (SK) Ca2+ -dependent K+ 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.