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. 2011 Aug 31;31(35):12593–12603. doi: 10.1523/JNEUROSCI.2397-11.2011

Figure 5.

Figure 5.

Decreased DA release in ventral and dorsal striatum of cKO mice. A, Graphical illustration of placement of DA-selective electrode for in vivo amperometric measurements in DStr and AcbC (bregma, 1.10 mm). B, Representative DA trace illustrating the calculation of redox ratio for each peak. C, G, DA amplitude, defined as the peak DA concentration (micromoles) from baseline in AcbC and DStr in response to four consecutive ejections of 120 mm KCl. D, H, trise, defined as time (seconds) between ejection and peak maximum (F, J), in AcbC and DStr for the four releases of DA. E, I, t80, defined as the time (seconds) from peak amplitude until the signal reached 20% of the peak amplitude (F, J), in AcbC and DStr for the four KCl-evoked releases of DA. F, J, Schematic illustrations of the first post-KCl ejection recordings of DA, based on graph values, for AcbC (F) and DStr (J). Insets show analysis of peak area, defined as area under curve. Four consecutive KCl ejections (numbered 1–4 on x-axes) were used, spaced by 5 min for DStr and 10 min for AcbC. AcbC data are from n = 7 Ctrl and n = 7 cKO mice. DStr data are from n = 11 controls and n = 12 cKO mice. Group data represent mean ± SEM. Significant main genotype effects observed by ANOVA analysis are illustrated by ##p < 0.01 and ###p < 0.001; differences by post hoc test are shown by *p < 0.05, **p < 0.01, and ***p < 0.001.