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. 2014 Apr 2;34(14):4929–4940. doi: 10.1523/JNEUROSCI.1423-13.2014

Figure 6.

Figure 6.

Expression of NKCC1 transcripts in the DLPFC of patients with schizophrenia and nonpsychiatric controls. We examined expression levels in the black group (AA) and white (CAUC) groups separately, comparing controls with patients with schizophrenia. In the black cohort, NKCC1b (1–27 (Δ21)) (**), 1–27 (21a) (*), 1–4a (*), and 1–2a (*) isoforms were significantly decreased in the DLPFC of patients with schizophrenia (NKCC1b: N = 28; 1–27: N = 27; 1–4a: N = 28; 1–2a: N = 27) compared with controls (NKCC1b: N = 31; 1–27: N = 30; 1–4a: N = 31; 1–2a: N = 30) (b–e). In the white cohort, the 1–2a isoform was also significantly decreased in patients with schizophrenia (N = 17) compared with controls (N = 14) (*) (e). There were no differences in the expression of NKCC1b (1–27 (Δ21)) (Control: N = 15; Schizophrenia: N = 17), 1–27 (21a) (Control: N = 15; Schizophrenia: N = 17), and 1–4a (Control: N = 15; Schizophrenia: N = 17) transcripts in the white cohort (b–d). There was no significant difference in the expression of NKCC1a (1–27) in either the black cohort (Control: N = 32; Schizophrenia: N = 28) or the white cohort (Control: N = 15; Schizophrenia: N = 17) (a).