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. Author manuscript; available in PMC: 2016 Jan 31.
Published in final edited form as: Neurobiol Dis. 2014 Dec 9;74:263–280. doi: 10.1016/j.nbd.2014.12.003

Figure 7. Administration of the NE inhibitor ZN200,355 to brain-injured NE KO mice confirms the functional benefits afforded by NE deficiency, without any confounding effects.

Figure 7

Injury-induced hyperactivity in the open field (a) was ameliorated to a similar extent in brain-injured untreated NE KO mice, brain-injured NE KO mice which received vehicle treatment, and brain-injured NE KO which received the NE inhibitor (1-way ANOVA p<0.0001; Dunnett’s analyses ****p<0.0001, ***p<0.001 and **p<0.01). Treatment with the NE inhibitor did not alter the response seen in untreated or vehicle-treated NE KO mice alone. WT data in (a) is reproduced from figures 4a and 6a, for comparison. NE inhibitor treatment also had no effect on brain-injured NE KO mice in terms of spatial memory retention in the MWM probe trials at the end of the testing period (b) and one week later (c), with both vehicle and NE inhibitor-treated NE KO mice showing preference for the target quadrant (1-way RM ANOVAs with Dunnett’s analyses). n=12–14/group.