Changes in synaptic density and myelination cannot be fully responsible for the observed developmental changes. Primarily, not all regions showing functional “connections” show monosynaptic anatomical connections. For example, non-human primates show robust rs-fcMRI connections between eccentric visual field representations in V1 (Vincent et al. 2007); this location lacks direct homotopic callosal connections (Newsome and Allman 1980). While an anatomic study of synaptic pruning shows an adult-like synaptic density in frontal cortex by age 16 (Huttenlocher 1990), there seems to be continued changes in rs-fcMRI connectivity in frontal cortex through the early part of the third decade (Fair et al. 2009; Dosenbach et al. 2010). Additionally, gross changes in myelination cannot explain the specific increases in functional connectivity between regions of adult networks, or decreases in connectivity between regions that continue to show increased myelination with development (i.e., prefrontal cortex). In fact, Supekar and colleagues found developmental increases in functional connectivity in the absence of increased fractional anisotropy, a DTI marker of myelination, although not myelination specifically (Supekar et al. 2010). Moreover, a modest amount of training in adults, which is
