We conducted qRT-PCR analyses for 2 genes whose expression was highly altered in the microarray analysis. Consistent with microarray data, the expression of GAD1, the gene encoding glutamate acid decarboxylase, a key enzyme for gamma amino butyric acid (GABA) synthesis, showed a significant increase in BPD L neurons. The decrease in the expression of SCN4B (encodes the beta subunit of voltage gated Type IV sodium channel) observed by microarray analysis was also seen as a reduction in L neurons of BPD cases by qRT-PCR, but this finding failed to reach statistical significance. SCN4B is known to regulate neuronal activity and appears to be especially important during brain development [49]. Changes in the expression of both of these genes have been reported in postmortem tissues from schizophrenia [50,51]. Thus the increase in GAD1 concurrently with a decrease in SCN4B indicates that BPD may be associated with an imbalance of excitatory and inhibitory neurotransmission in developing neurons. Interestingly, postmortem data on autopsied hippocampus indicate a decrease in GAD1 mRNA in BPD patients [11]. These data raise the question whether the increase in
