ABSTRACT

Critically Depend upon Vigilance States ......................................... 160 7.6 Conclusions and Future Challenges .............................................................. 163 Acknowledgments .................................................................................................. 164 References .............................................................................................................. 164

The basal ganglia (BG) are a recipient for cortical information. Cortical projections to the BG are composed of two distinct pathways, the corticostriatal (CS) and corticosubthalamic systems, which connect monosynaptically the main input nuclei of the BG by glutamatergic synapses (Charpier et al. 2010; Wilson 2004). The striatum receives inputs from nearly all functional subdivisions of the cortical mantle, including neocortical and allocortical areas. These cortical inputs are topographically ordered and processed by the GABAergic striatal projection neurons, the main (∼90%) neuronal population in the striatum morphologically de’ned as medium-sized spiny neurons (MSNs) (Chang et al. 1982) (see Figure 7.2A), and by most of the striatal interneurons which, in turn, modulate the responsiveness of MSNs (Kreitzer 2009). Two main CS macrocircuits can be outlined according to their different global functions. Whereas the “limbic” hippocampal (and prefrontal cortex)-ventral striatal subsystem has been delineated to mediate motivational and reward processes, the CS subsystem implicating the dorsolateral part of the striatum is involved in the correct completion of sensorimotor behaviors and is essential for learned motor sequences to become habitual (Graybiel 1995, 2008; Chapter 9). The cortical information processing in these two striatal functional subsystems is under an extrinsic modulatory control mediated by afferent dopaminergic ’bers originating from the ventral tegmental area and substantia nigra pars compacta (Wilson 2004). Consistent with their normal behavioral functions, abnormal activities in CS systems are implicated in various neurological disorders related to action compulsion (such as obsessive compulsive disorders and drug addiction) and action disability (such as Parkinson’s disease [PD] and Huntington’s disease) (Graybiel 2008; Chapter 10). Thus, understanding how cortical inputs are processed by MSNs and transformed into behaviorally relevant outputs is a decisive challenge for the elucidation of the cellular basis of normal and pathological functions related to the BG.