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. Author manuscript; available in PMC: 2016 Sep 12.
Published in final edited form as: Prog Neurobiol. 2015 Apr 9;130:1–28. doi: 10.1016/j.pneurobio.2015.03.004

Fig. 11.

Fig. 11

A hypothesis of disrupted development that could underlie disorders of cortical circuit development associated with 22q11DS. (Left) A schematic of normal development indicating normal mechanisms of basal progenitor proliferation that insure appropriate numbers of layer 2/3 projection neurons as well as migratory mechanisms that mediate appropriate placement of key subsets of GABAergic interneurons. (Left middle) Changes in layer 2/3 projection neuron frequency lead to diminished corticocortical connectivity normally made by these neurons, while local alterations in excitatory/inhibitory balance due to disrupted migration and placement of GABAergic interneurons modifies local processing of information in layer 2/3. (Right middle) These changes lead to under-connectivity, especially between cortical association regions in the LgDel mouse. (Right) Similar changes may lead to underconnectivity in frontal, parietal and temporal association cortical regions in 22q11DS patients.