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

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© 2014 Huang et al

This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.

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The mean values of dopamine signal evoked by 1 Pulse/25 Hz, 10V stimulation intensity of the 6-Pa-injured group is plotted in panel A, and by 10 Pulses/25 Hz, 10V stimulation intensity of 6-Pa injury group is plotted in panel B. There is a significant suppression in injured animals (open box bar) in each time point compared with the control group (gray bar) (p<0.05*, t-test). In the amantadine therapy group (black bar), the signal decreased initially 1 week later and increased 2 weeks after injury. The maximum value of the signal of dopamine release at each time point after injury in the control (solid circle), 6-Pa-injured (open circle), and amantadine therapy (open square) groups are plotted in panel C, which showed that the significant increase in amantadine therapy animal while comparing with 6-Pa injured animal; and there was no significant difference between control and amantadine therapy group. (Note: *indicates p<0.05; **indicates p<0.01; and ***indicates p<0.001).