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. Author manuscript; available in PMC: 2012 Jun 1.
Published in final edited form as: Biol Psychiatry. 2011 Apr 13;69(11):1043–1051. doi: 10.1016/j.biopsych.2011.02.013

Figure 3.

Figure 3

In vivo CREB activity in ENT1−/− mice. (A) No changes in CREB protein expression but (B) decreased phospho-CREB (Ser133) expression in ENT1−/− mice by Western blot analysis [t(14) = 4.8, p < 0.001]. n = 8 for each genotype; *p < 0.05 compared to ENT1+/+ mice after normalization by GAPDH (unpaired, two-tailed t-test). (C) Representative NAc core coronal brain sections of β-galactosidase (lacZ) expression by X-Gal staining. Scale bar = 100 µm. Decreased CRE-driven lacZ expression in the NAc core of CRE-lacZ/ENT1−/− mice compared to CRE-lacZ/ENT1+/+ mice [t(14) = 3.80, p = 0.002]. n = 8 for each genotype; *p < 0.05 compared to CRE-lacZ/ENT1+/+ mice by unpaired two-tailed t-test. (D, E) Regulation of CREB activity by ENT1 inhibition. (D) CRE-lacZ/ENT1+/+ mice showed decreased CREB activity by ENT1 inhibition by 50 µM NBTI microinjection to the NAc core [t(18) = 3.7, p = 0.002]. Representative NAc core coronal brain sections of lacZ expression after NBTI treatment by microinjection on CRE-lacZ/ENT1+/+ mice. Scale bar = 100 µm. (E) CRE-lacZ/ENT1−/− mice showed no further effects of ENT1 inhibition. Representative NAc core coronal brain sections of lacZ expression after NBTI treatment in CRE-lacZ/ENT1−/− mice. Scale bar = 100 µm. n = 10 for each genotype; *p < 0.05 compared to their saline-treated groups by unpaired two-tailed t-test. AC, anterior commissure. All data are presented as mean ± SEM.