Figure 6. Pathway bias and neuromodulatory control of SPN excitatory synaptogenesis during development.
(A) Schematic summarizing the key result of this study. Neuromodulation, acting via PKA, regulates glutamate-dependent developmental synaptogenesis. (B) These results fit into the larger framework of the basal ganglia model, which indicates that through polysynaptic recurrent loops involving the neocortex, dSPN activity is positively coupled to striatal glutamate release onto SPNs of both pathways, whereas indirect pathway activity provides negative feedback. (C) Together the two models can account for a transient developmental bias towards the earlier innervation of dSPNs over iSPNs. During development, dSPNs have greater dendritic spine density and miniature EPSC frequency but not amplitude, compared to iSPNs. These graphs represent re-analyses of control data from a previously published study (Kozorovitskiy et al., 2012).