Insights to disturbed connectivity in schizophrenia have been provided by MRI, postmortem, and animal studies. Alterations in GABAergic and n-methyl-D-aspartate receptor (NMDAR)-mediated transmission display a common neurobiological background of connectivity deficits revealed by TMS/EEG/MEG. First, studies on human brain tissues showed lower GABA-related transcripts in four cortical areas in schizophrenia patients [21]. Second, the results of different TMS-studies using specific paradigms to investigate inhibitory intracortical networks point toward a GABAergic dysfunction in the motor system of this patient group [44]. Third, schizophrenia patients show a reduction in the mRNA expression of the GABA-synthesizing enzyme, GAD67, and a reduction in GABAergic interneurons in several cortical areas [2, 27].
