Abstract
Corticostriatal afferents can engage parvalbumin-expressing (PV+) interneurons to rapidly curtail the activity of striatal projection neurons (SPNs), thus shaping striatal output. Schemes of basal ganglia circuit dynamics generally consider striatal PV+ interneurons to be homogenous, despite considerable heterogeneity in both form and function. We demonstrate that the selective co-expression of another calcium-binding protein, secretagogin (Scgn), separates PV+ interneurons in rat and primate striatum into two topographically-, physiologically- and structurally-distinct cell populations. In rats, these two interneuron populations differed in their firing rates, patterns and relationships with cortical oscillations in vivo. Moreover, the axons of identified PV+/Scgn+ interneurons preferentially targeted the somata of SPNs of the so-called 'direct pathway', whereas PV+/Scgn- interneurons preferentially targeted 'indirect pathway' SPNs. These two populations of interneurons could therefore provide a substrate through which either of the striatal output pathways can be rapidly and selectively inhibited to subsequently mediate the expression of behavioral routines.
Highlights
Interactions within and between populations of interneurons and spiny projection neurons (SPN) of striatum are critical for the expression of many basal ganglia-dependent behaviors
Our findings suggest that distinct subpopulations of PV+ interneurons could enable corticostriatal afferents to orchestrate SPN activity in a topographically- and output pathwayselective manner
All striatal Scgn+ cells co-expressed the ‘pan-neuronal’ marker Neuron-specific nuclear antigen (NeuN), but not the SPN-specific marker Ctip2 (Arlotta et al, 2008) (Figure 1A,B), indicating that Scgn is exclusively expressed by interneurons
Summary
Interactions within and between populations of interneurons and spiny projection neurons (SPN) of striatum are critical for the expression of many basal ganglia-dependent behaviors. Striatal PV+ interneurons can form axo-somatic synapses with SPNs (Koos and Tepper, 1999; Kubota and Kawaguchi, 2000), allowing them to powerfully inhibit SPNs of both the so-called ‘direct pathway’ and ‘indirect pathway’ (Gittis et al, 2010; Planert et al, 2010). These interneurons exhibit short-latency responses to powerful excitatory inputs from afferents originating in distinct cortical areas (Ramanathan et al, 2002; Sharott et al, 2012), providing a mechanism for rapidly stopping or delaying SPN spiking (Mallet et al, 2005) and, in turn, modulating striatal outputs.
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