Abstract
Anatomical and physiological studies have led to the assumption that the dorsal striatum receives exclusively excitatory afferents from the cortex. Here we test the hypothesis that the dorsal striatum receives also GABAergic projections from the cortex. We addressed this fundamental question by taking advantage of optogenetics and directly examining the functional effects of cortical GABAergic inputs to spiny projection neurons (SPNs) of the mouse auditory and motor cortex. We found that the cortex, via corticostriatal somatostatin neurons (CS-SOM), has a direct inhibitory influence on the output of the striatum SPNs. Our results describe a corticostriatal long-range inhibitory circuit (CS-SOM inhibitory projections → striatal SPNs) underlying the control of spike timing/generation in SPNs and attributes a specific function to a genetically defined type of cortical interneuron in corticostriatal communication.
Highlights
It is very well established that cortical neurons regulate the activity of spiny projection neurons (SPNs) in the striatum through long-range glutamatergic/excitatory projections (Landry et al, 1984; Wilson, 1987; 2004; Graybiel et al, 1994; Lovinger and Tyler, 1996; Reiner et al, 2003; Kress et al, 2013), while inhibition is mediated by local feed-forward and feed-back circuits
Anatomical and electrophysiological properties of corticostriatal somatostatin neurons To visualize long-range GABAergic projections originating in the cortex and terminating in the dorsal striatum, we conditionally expressed GFP in somatostatin-expressing (SOM) interneurons by injecting AAV.GFP.Flex into the right auditory cortex (AC) of SOM-Cre-tdTomato transgenic mice (Figure 1a)
GFP was colocalized with SOM/tdTomato-expressing neurons in the AC (Figure 1b left) and GFP-positive axons were visible in coronal sections of the right dorsal striatum in these mice (Figure 1b middle and right)
Summary
It is very well established that cortical neurons regulate the activity of spiny projection neurons (SPNs) in the striatum through long-range glutamatergic/excitatory projections (Landry et al, 1984; Wilson, 1987; 2004; Graybiel et al, 1994; Lovinger and Tyler, 1996; Reiner et al, 2003; Kress et al, 2013), while inhibition is mediated by local feed-forward and feed-back circuits (for review [Tepper et al, 2008]). Anatomical studies using retrograde tracers and immunohistochemistry have proposed that between 1–10% of the GABAergic ’interneurons’ in rodents, cats, and monkeys give rise to long-range corticocortical projections (McDonald and Burkhalter, 1993; Tomioka et al, 2005; Higo et al, 2007; Tomioka and Rockland, 2007; Higo et al, 2009). A previous study has demonstrated the presence of a corticostriatal GABAergic projection (Tomioka et al, 2015), but the cells of origin and physiological function of this GABAergic projection from the cortex to the dorsal striatum were not explored
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