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. 2014 Jan 30;9(1):e86354. doi: 10.1371/journal.pone.0086354

Figure 1. The input/output curves of the evoked dopamine release at 1 (▴, 4 rats, 1 week after injury), 2 (♦, 3 rats, 2weeks after injury), 4 (△, 3 rats, 4 weeks after injury), 6 (□, 3 rats, 6 weeks after injury), and 8 (○, 3 rats, 8 weeks after injury) weeks after injury compared with the control animal group (•) are summarized.

Figure 1

Dopamine release was severely suppressed in the fluid percussion injury group under either 1P (A) or 10P (B) stimulation. Amantadine pumping infusion therapy reversed the dopamine-release deficit 2 weeks later (C, solid square ), and the releasing signal even larger than control group under 1 P stimulation (C) at 4 weeks (△, 3 rats, 4 weeks after injury) later and increasing occurred since 2 weeks () after injury at 10 pulses-stimulation (D). The inset panels on the right side show representative cyclic voltammetry (CV) trace (upper) and dopamine signals (lower) (A and B: Control (solid line) vs. 6-Pa group (dotted line) at 8 weeks post injury; C and D: Control (solid line) vs. 6-Pa with amantadine therapy (dotted line) at 8 weeks post injury). (Note: *indicates p<0.05; **indicates p<0.01; and ***indicates p<0.001).