ABC Transporters in Neurogenesis Figure 8. Lack of ABCB1 or ABCC1 expression leads to impaired exploratory activity. The diagrams show Y-maze-related parameters. Plotting the animals’ course in the Y-maze, the running distance reveals a significant decrease in ABCB1- (213%) and ABCC1- (217%) deficient animals (A), while this parameter was only slightly, non-significantly decreased in ABCG2-deficient mice. The same behavioral pattern was detected for exploratory activity as assessed by the arm entries (ABCB10/0 216%; ABCC10/0 223%) (B). Error bar: SEM, *p,0.05. doi:10.1371/journal.pone.0035613.g008 ABCC1 did not affect expression of ABCB1b or ABCG2. While previous studies have not found regulatory mechanisms between ABC transporter expression by analyzing whole brain homo- genates [51,52], we show NSPC-specific regulatory mechanisms in ABC transporter mRNA expression for the first time. It is conceivable that these regulatory effects account for the altered proliferation capacity in ABCG20/0 strains due to altered ABC transporter expression profiles, increasing the cells’ capability to cope with the cell culture environment. These cell-intrinsic effects are so specific to environmental parameters of the in vitro situation that this effect may be simply overwhelmed by the far-ranging effects of altered brain homeostasis due to ABC transporter- deficiency, leading to the effects observed in vivo. The CCI model impairs the relatively isolated (privileged) state of the brain by disrupting the blood-brain barrier. Following trauma, metabolites from the bloodstream can directly access and influence the previously protected stem cell pools. The excretion functions of ABC transporters are also highly taxed to maintain Figure 9. ABC transporter deficiency promotes anxiety. The diagrams show parameters assessed via the elevated plus maze. Mice deficient for ABCB1 (244%) and ABCG2 (232%) showed a significantly decreased presence in the open arms (A). The time of residence in the closed compartments was significantly increased in all ABC transporter-deficient mouse strains (ABCB10/0 +43%; ABCG20/0 +24%; ABCC10/0 +32%) (B). Running speed (celerity) in the open arms was not changed in any of the ABC transporter-deficient mice (C). ABCB1 (223%) and ABCC1 (214%) transporter-deficient mice showed significantly lower celerity values in the closed arms (D). Error bar: SEM, *p,0.05; **p,0.01; ***p,0.001. doi:10.1371/journal.pone.0035613.g009 PLoS ONE | www.plosone.org 9 April 2012 | Volume 7 | Issue 4 | e35613