Previous reports have highlighted disruption of brain regulatory mechanisms in MDD, focusing on “hubs” of the mood regulatory network such as the rostral anterior cingulate (rACC) [85] or the dorsal nexus posited by Sheline and colleagues [20]. Disruption of normal connectivity patterns could explain many of the regulatory, cognitive, neurovegetative, and emotional symptoms of MDD [75], [86]–[87]. It remains unclear what fundamental mechanism underlies and perpetuates network dysregulation. The current results are consistent with a growing body of literature implicating disturbed brain oscillatory activity in the pathogenesis of MDD [42], [88]–[90]. Modulation of cerebral oscillatory activity plays a central role in regulation of mood, and processing of affective information and emotional stimuli [91]–[93]. Interestingly, synchronization of oscillatory activity is strongly influenced by central serotonergic tone [89]. Serotonergic projections from the medial septal area inhibit hippocampal theta oscillatory synchrony [94], while alpha synchrony is modulated by serotonergic projections from the raphe nuclei to the intralaminar and medial thalamic nuclei [95]. Furthermore, oscillatory activity and related behaviors are modulated by administration of antidepressant medication in animals [94], [96]–[97]. Oscillatory synchrony could represent
