EEG synchronization deficits may index disturbances of GABAergic neurotransmission. Decreased GABA transmission, glutamate receptor expression, and glutamic acid decarboxylase, an enzyme involved in GABA synthesis and regulation, have been implicated in BD (Benes and Berretta, 2001; Beneyto et al., 2007; Brambilla et al., 2003). Several studies have shown compelling evidence of GABAergic modulation of alpha activity. Fingelkurts et al (2004) found that EEG alpha activity was affected by administration of lorazepam, a GABA agonist, in healthy adults. They suggested that GABA signaling can reorganize the neuronal dynamics in alpha band in terms of local and remote functional connectivity. In addition to lorazepam which can reduce alpha activity (Ahveninen et al., 2007), diazepam has also been reported to reduce the eye-closure induced alpha power in MEG recording (Hall et al., 2010). Therefore, the disturbance of EEG synchronization in this study, resulting in the topological alteration of brain network, may reflect dysfunction of GABAergic interneurons in BD patients (Benes and Berretta, 2001). An interpretative issue is the possible effect of medication on GABAergic transmission and EEG activity. Because anticonvulsant mood stabilizers as
