A GABA-to-GABA mechanism has been suggested in schizophrenia by postmortem studies showing a decrease of interneurons in sectors CA2 [9], particularly those containing parvalbumin [44], [45]; a compensatory upregulation of GABAA receptor binding activity was also detected on interneurons in CA2/3, but not pyramidal cells [46]. This evidence concerns the gene PVALB and schizophrenia.