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. Author manuscript; available in PMC: 2013 May 1.
Published in final edited form as: Neurobiol Aging. 2011 Apr 30;33(5):1001.e7–1001.e16. doi: 10.1016/j.neurobiolaging.2011.03.022

Fig. 3.

Fig. 3

Slower decay time of DA signals in Nurr1 +/− mice slices. (A) Comparison of the decay time of the DA signals obtained from the control (Ctrl, gray) and Nurr1 +/− mice (black). The times when the DA signals decay to 90% of the peak (t90) are shown for each representative trace (filled circles). (B) The t90 was significantly longer in Nurr1 +/− mice (black bar) compared to the control (n = 30, 38; ** p < 0.01). (C) Example of normalized DA signals (100% of control amplitude) showing the longer decay time in Nurr1+/− mice (black trace) compared to the control (gray trace). (D) Blocking the DA transporter with GBR (2 μM) abolished the difference in decay of the control and Nurr1 +/− DA signals (shown in C). The peak amplitudes were again normalized to the control’s peak. (E) When DATs were inhibited by GBR, the difference in peak DA amplitude is accentuated between the control (gray) and the Nurr1+/− (black) mice. (F) The average peak DA amplitude was large and significantly different between the two genotypes (n = 10, 15; ** p < 0.01).